Hey all you hairy beasts.
The point of this lengthy post is to educate you about androgenetic alopecia, versus other types of hair loss, as well as how hair actually grows and is lost. This info will be a helpful knowledge base for understanding later sections.
Some of this may not seem to be completely pertinent to AAS associated hair loss, but in a way it all is.
Some of this is cut and pasted, but it is all original and written by me: from a short book I wrote on the subject. There is also a focus on medical and especially surgical hair restoration, which may or may not interest you.
Scientific Basis of Hair Growth and Distribution
In the following discussion, we will mostly be concerned with scalp hair. Although scalp and body hair share many of the same characteristics, it is balding that we seek to understand and remedy, so this will be the focus unless otherwise indicated.
Hair is a living entity, although the shafts we see are largely the extension, outside the body, of a dead protein called keratin. Beneath the level of the skin, however, there sits a powerhouse of cellular activity. This cell division and differentiation pushes the hair shaft outward; thus we see hair growth that averages about one half inch per month.
There are two types of hair: terminal and vellus. The terminal hairs are the thick, strong, usually pigmented ones that constitute the greatest volume of our hair. The vellus hairs are the very fine, short, lightly pigmented hairs, sometimes called “baby hairs”, that can be often detected around the hairline, and throughout the scalp, as well as the light “fuzz” elsewhere on the body. This difference is significant when discussing balding, for in balding, the terminal hairs gradually undergo a metamorphosis called “miniaturization”. They become shorter, finer, and less colored; in short, they become vellus hairs. If you look closely at the heads of balding men, you will see that, in many of the areas of balding, the strong terminal hairs are replaced by these fine, vellus, “baby” hairs; this is miniaturization, and we will discuss this in greater detail in the next section on hair loss.
In addition to these two types of hairs, the individual characteristics of the hair are very important in determining appearance (including the appearance of balding) and styling options. These characteristics include color, curl or kink, caliber (cross-sectional area) and density (number of hairs per unit area). For example, although African hair tends to have a lower density (hairs per square inch) than Caucasian hair, its extreme curliness lends it a great volume and ability to achieve coverage after hair transplant surgery. Asian hair, although it tends to be very coarse (high caliber), may be more challenging to transplant due to the straight nature of the hair, and the contrast between dark hair and lighter skin. However, these are but a few examples, and all of these characteristics are taken into account by the hair restoration expert in designing a program for each unique individual. This is where the art of hair restoration meets the science.
In addition to the hair shafts themselves, there are other structures involved in the growth and function of hair. Each hair is associated with a sebaceous gland, which produces the oily sebum that serves to lubricate the hair shafts. Likewise, there is an erector pili muscle, which contracts to raise the hair in situations of anger, fright or cold. Although this function serves little purpose in humans, we see it in other mammals when their “hackles” rise.
Hair growth and rest occurs in three phases: anagen, catagen and telogen. The anagen phase is the period of active growth. At any time, about 85 to 91% of hairs are in this active, anagen phase. Anagen may last from 2 to 7 years, but usually about 3 years on average. The catagen phase is considered transitional, and the telogen phase is the dormant, or resting phase. When the hair enters the telogen stage, the hair is either pulled out during normal grooming, or is pushed out when the new hair shaft growth begins.
Last, but certainly not least, is the anatomical and physiological unit we have come to call “follicular units”. If you have done any current reading on hair restoration surgery, you have surely come across this term. Believe it or not, it was only in the early 1980’s that it was recognized that hairs grew not as strictly single shafts, but as discrete groups of one, two, three, four, and rarely five terminal hairs. These hairs are joined by one or two vellus hairs, a sebaceous gland, an erector muscle, a neurovascular bundle (meaning the nerve and blood vessels), and the perifolliculum, or fine connective tissue sheath. These units are easy to see emerging from the skin under slight magnification on cross section through the skin (figure 1) or when the hair is clipped short (figure 2).
Sorry, Pix wouldn't load!
Figure 1 (cross section)
Figure 2 (surface of scalp)
The significance of recognizing follicular units as the fundamental grouping of scalp hair cannot be underestimated. This understanding has led to a revolution in the techniques of modern hair transplantation. The past decade has given us a whole new perspective on the harvesting, movement and implantation of permanent hair into areas of balding scalp. This can now be done, at least by well-trained surgeons and their operative teams, in a manner that is natural and undetectable. We will discuss this more, in greater detail, in later sections.
OK, now this part's essential for a full understanding of hair loss. There are LOTS of myths about balding (some of which I've seen promulgated on this board! Tsk, tsk!)
Hair Loss: Causes and Conditions
There are many causes of hair loss in men and women, including disease, nutritional deficiency, hormone imbalance, and stress. However, by far the most common cause is what is called adrogenetic alopecia. Alopecia is simply the medical term for hair loss. Androgenetic refers to the fact that both a genetic predisposition to balding, and the influence of androgens, or male hormones, play a part in this type of hair loss.
In fact, there is a third factor, which is the passage of time, or aging. In other words, in order for androgenetic alopecia to occur, there must be:
1) a genetic propensity for balding
2) the presence of androgens, or male hormones
3) enough aging time to allow the first two factors to exert their influence on the hair follicles
Genetics is not always simple, and such is the case with balding. Just the presence or absence of balding in one’s parents or grandparents, on either the mother’s or father’s side, is not necessarily predictive of one’s likelihood of balding. Certainly, if a man’s father is completely bald, and this man begins to rapidly lose hair in his early twenties, it’s a safe bet that he will develop extensive balding at some point. In short, it’s very hard to accurately predict who will go bald and how rapidly.
This inherent uncertainly about the progression of balding is of utmost importance in planning surgical hair restoration, as we will see in later sections. We must always plan for a “worst case scenario” in order to give patients the best possible results in the long term, as well as in the short term. Anything less is irresponsible.
All normal men and women produce “male” hormones. The most common of these are testosterone, androsteinedione, and dihydrotestosterone (DHT). Androgens are produced by the testicles and adrenals in men, and by the ovaries and adrenal glands in women. These hormones are quite important in both sexes, but occur in different concentrations, being much more predominant in males than in females. This, in part, is responsible for the typical differences between the genders.
It is the exposure of the hair follicles to DHT, in a genetically susceptible person, over a period of time, which leads to androgenetic alopecia, or male and female pattern baldness. How does this exposure to DHT occur?
In certain cells of the hair follicle, and in the sebaceous glands, there are high levels of an enzyme called 5-alpha-reductase. What this enzyme does is to convert testosterone, which is delivered to these areas by the blood, into DHT. This is important not only in understanding the mechanisms of balding, but also one medical treatment now available: Propecia (finasteride). What Propecia does is inhibit, or limit the activity of, this 5-alpha-reductase enzyme. Therefore, there is less conversion of testosterone to DHT, and lower levels of DHT are found in the follicle. In later sections, we will discuss this and other medical treatments in much greater detail.
There is no set age at which balding occurs. It is a process, and this is a simple, but oft-ignored fact. Like any process, it can be rapid or slow, it can begin toward the end of life or in the late teens, and it can progress in a predictably inexorable fashion, or it can stop and start, seemingly stabilize, and then begin again. Once we understand and accept this as a dynamic process, then we can better plan for the present and for the future in terms of how we treat it. This quest for understanding, which you have begun just by opening this book, will do more than all the despairing thoughts, hand-wringing, and self-pity, toward allowing a clear-eyed, rational, long term approach to the problem of hair loss.
So we now have looked at these three interdependent factors that play into the common types of balding. Again, they are: hormones, genetics, and Father Time. So what exactly does happen to the hair? Let’s take a look.
Assuming we have a genetically predisposed person, then as the follicles are continuously exposed to DHT, an interesting phenomenon occurs. Remember the anagen phase, or active growth phase of the hair? This phase becomes gradually briefer and briefer, and eventually the hair becomes finer and shorter, and less deeply colored. We call this “miniaturization” of hairs. This is also the point at which hair loss tends to first be noticed. It’s not that there are fewer hairs on the head, but that their caliber (cross-sectional area), color and length are so diminished that they no longer provide “coverage” for the scalp beneath. Light penetrates through to the shiny scalp, and this is perceived by the observer as “thinning” or balding.
Also, the ratio between hairs in the anagen phase and those in the telogen, or resting phase, is increased. This simply means that, at any given time, an increased number of hairs are in the telogen phase. These extra numbers of telogen hairs will be found in the susceptible zone for common balding, which is the front, top, and crown of the head. The so-called “permanent” zone, the familiar horseshoe-shaped wreath of hair around the back and sides, is unaffected by these changes. The telogen hairs are easily dislodged during washing, drying, or combing, and this is the second sign of balding: in addition to the apparent thinning seen with miniaturization, we begin to see larger numbers of hairs on the comb, the towel, the pillowcase, or in the bathroom drain. This can be quite traumatic, especially for the younger man or for women. In the next section, we will discuss the natural history of balding, that is, the way it first presents or appears, the different ways it progresses, and how it affects the different regions of the head.
For the sake of completeness, let’s briefly mention some of the other patterns of hair loss, if only to distinguish them from androgenetic alopecia (male and female pattern baldness). There is alopecia areata, where discrete patches of scalp go bald; triangular alopecia, which tend to occur in a triangular pattern in the temporal area; alopecia universalis, in which the entire body may be affected; and various “toxic” alopecias, including those following a severe illness, sometimes with high fever, or following pregnancy. Toxic alopecias may also occur with low thyroid and/or pituitary gland function, or following chemotherapy. The cicatricial (scarring) alopecias occur following tissue destruction and inflammation.
Also seen are the so-called diffuse alopecias (patterned and unpatterned), in which there is widespread thinning that may affect the “permanent” zone as well as the areas vulnerable to balding. In any or all of these less common types of balding above, it may be necessary to have a complete physical and laboratory workup, possibly including scalp biopsy.
So again, the common types of balding are directly related to the presence of male hormones in a genetically predisposed person over time. This can occur in both men and women. The process involves progressive miniaturization of the terminal hairs, and diminished length of the active hair growth cycle. Now, let’s take a look at how this microscopic, cellular process is manifested on the head; we can call this the natural history of balding.
Stay tuned: much more to come! The following statement about A.A. (MPB) is the "take-home" message for this section!
Like any process, it can be rapid or slow, it can begin toward the end of life or in the late teens, and it can progress in a predictably inexorable fashion, or it can stop and start, seemingly stabilize, and then begin again.
The Natural History of Balding
The natural history of balding is simply the way it first presents or appears, the different ways it progresses, and how it affects the different regions of the head. We consider it vital that anyone with common balding become familiar with these concepts. If you can become as conversant as possible with the different balding patterns, and can learn to compare and contrast your own hair loss with these known patterns, you will become a more informed patient. You will ask better questions, understand the answers in more depth, and be more likely to take care of the hair that you do have. Also, if you choose a medical or surgical hair restoration treatment, you will most likely have appropriate expectations, and be more apt to follow the doctor’s instructions about post-operative care or taking your medications.
In the beginning, we are born with varying amounts of soft, fine baby hair, which is vellus in nature. As we grow, much of our hair becomes the more robust terminal type. It may change in pigmentation, often becoming darker, and it may acquire a curl or wave, and may become coarser.
After puberty, we see what we call the adolescent hairline. This type of hairline may only persist for a few years, and is characterized by its low, fairly flat spread across the forehead. This looks great on teenagers, but this is rarely found on mature adults, even in their twenties.
As men progress through their twenties, given that there is no balding, the hairline assumes the “mature” look, with slight frontal-temporal recessions, which impart a concave appearance to the hair line on each side, with a lower peak in the middle. This is analogous to the number “II” Classification on the Norwood scale (fig. 3). This is the most well known of several systems for classifying degrees of baldness, and was developed by Dr. O’Tar Norwood. This is a very useful scale for identifying one’s own current degree of hair loss in a way that is acknowledged and understood by physicians in the field of hair loss treatment.
This “mature” hairline is not considered balding; the Norwood III is considered the first evidence of balding in androgenetic alopecia (male pattern baldness). In studying the Norwood charts, we see that usually the most advanced balding is known as a class VII, and that there are also Type “A” variants in which the forelock in the middle tends to recede along with the fronto-temporal areas, and in which there is be less overt crown loss than in the regular III, IV, and V patterns.
Figure 1 (sorry again!)
So there may be front-to-back hair loss, or hair loss beginning in front and at the crown simultaneously, or sometimes isolated vertex or crown loss (the “bald spot”). These patterns are often overlapping and not as clear-cut as in the drawings on the chart, but they are an adequate and useful guide. It is important to understand that a person may be a III at age 25, but have progressed to a V or VI by age 35. Anyone considering surgical hair restoration needs to understand the unpredictable nature of the balding process; if further loss is not planned for, then what may be a nice cosmetic effect at one age can become a cosmetic nightmare ten years down the road. We will devote an entire, later section to just this kind of strategic planning.
A word about women’s hair loss: women can experience a Norwood type of hair loss pattern. More often, however, they experience a relative sparing and preservation of the frontal hairline, but have diffuse thinning on the top of the scalp. There is also a classification system for women known as the Ludwig Classification (figure 4).
Figure 2 (!!)
Sometimes women are candidates for surgical hair restoration due to balding, and at times have lost hair due to other cosmetic procedures, like face-lifting. This hair loss is often around the hairline or ears, and can be remedied. Women may also experience “traction alopecia”, which is caused by the chronic tugging force of tight braids or pigtails. This type of loss is also amenable to transplantation.
We have attempted here to stress the relative unpredictability of “pattern” baldness. This must be reemphasized. Often, young men seek hair transplantation and have desires or illusions about how they would like to appear. These may or may not be feasible. Certainly, when one is 25, it may be hard to care about one’s appearance at 45, but this must be factored into the equation. The recent memory of the low, adolescent hairline burns brightly in the mind of a young man, but a really good hair transplant procedure should always give the patient results that can be “worn” for a lifetime, and always appear appropriate for that individual’s age and head shape. This is where the attention of an experienced, well-trained, aesthetically sensitive hair restoration surgeon makes all the difference in the world.
Medical Treatments for Hair Loss
This section is bound to upset some people. They will feel that their favorite hair loss preventative has been slighted. However, the section below is NOT saying that topical spironolactone, Nizoral shampoo, or other treatments do not work. What it IS saying, is that from a scientific perspective of rigorous, double-blinded, placebo-controlled trials, we “know” that finasteride and minoxidil are proven to work. How well? Not perfectly, that’s for sure. (Besides, I wrote this, and I use Nizoral 3 times a week). So here’s the information, take it with a grain of salt!
For thousands of years, hopeful and desperate men have fallen prey to hucksters and salesmen hawking various potions and ointments, with claims of miraculous balding cures. The latest and greatest cures have never lived up to their hype, leaving the balding victims poorer but (sometimes) wiser. A powerful placebo effect (based on a strong desire for the treatment to work), along with gullibility or desperation, often resulted in a temporary sense of “improvement”. Eventually, however, the fact that there were no cures for baldness became evident.
Even today, we have no miracle “cures” for baldness. Even surgical hair restoration does not cure the balding process; what it does is redistribute permanent hair to balding areas. The same can be said of the two medical or drug treatments that have been shown to be of use in hair loss. Propecia, and especially Rogaine, do not so much reverse balding, but halt or slow its progression.
Minoxidil has been available in oral form for years. It was originally developed as an agent for treating high blood pressure; it had a number of significant side effects, which limited its use to people with severe, refractory high blood pressure, which was not completely responsive to combinations of other medications. One of the less dangerous, but quite obvious, side effects was “hypertrichosis”, or the growth of hair on the face or other areas of the body.
Of course, someone had the bright idea that perhaps applying this drug to the bald scalp might grow hair there. Thus, Rogaine was developed by The Upjohn pharmaceutical company, and the rest is history. Again, Rogaine does not cure baldness; in fact, no one is quite sure how it works. We do know that it does not grow hair on completely bald scalp; rather, it tends to retard the loss of hair in areas that are highly miniaturized. It may be that Rogaine prolongs the growth phase of the hair (remember the anagen cycle, that gets progressively shorter in the balding process), which halts or slows the miniaturization process.
With the use of Rogaine, it may take 6 to 12 months to notice a change; in fact, some people do not notice a difference unless they stop using it. Within 2 to 3 months of discontinuing the medication, any “regrowth” or appearance of increased density will vanish. In other words, even if Rogaine works for you, you must continue the medication indefinitely, or any benefit will be lost. Also, it is effective in the crown or top of the head, but not in the frontal area. This is unfortunate, because the front of the scalp and the hairline are the most cosmetically important areas. (Please repeat after me! The utmost importance of this primary rule of hair restoration will be reemphasized over and over as we consider treatments for balding).
Rogaine also must be used twice a day; once a day application has been clearly shown to be ineffective. In addition, the growth may not be as great as one imagines; since Rogaine probably works by increasing the thickness of hairs which are already miniaturized, the most many patients see is an apparent growth of fine, fuzzy hair which does not tend to grow very long.
Women may also benefit from the use of Rogaine, especially since their hair loss is often characterized by diffuse thinning. If this is the case, a halting or reversal of thinning may be possible with prolonged use; but as with men, stopping the medication will result in a reversal of the benefits.
Some hair restoration surgeons recommend that their transplant patients use Rogaine before and then immediately after the surgery, especially is grafts have been placed in and around existing hair. The medication may help prevent the temporary loss of healthy, preexisting hair due to the shock of the procedure. Some surgeons do feel that the medication should be stopped a week prior to the surgery, because it dilates blood vessels, and might increase operative bleeding.
The drug finasteride (marketed as Proscar for symptoms of prostate enlargement) has been available for years. Only since 1998 has it been approved for use in male pattern balding, and has been formulated as an oral, one milligram tablet called Propecia (versus the five milligram Proscar).
This drug works by inhibiting the action of the enzyme 5-alpha-reductase, which, as you remember, is the enzyme responsible for converting testosterone to dihydrotestosterone (DHT). Men with pattern balding have higher levels of this enzyme in and around the follicles that are at risk for loss. It is the effect of DHT on the hair follicles that leads to the miniaturization of terminal hairs. So, if we inhibit 5-alpha-reductase, then we inhibit DHT formation, decrease its levels in the blood stream and in the scalp, and stop or slow the process of miniaturization that we know as balding. Indeed, this is what was found in the clinical studies on Propecia.
A word about hormone effects: DHT is responsible for facial hair growth, increased incidence of acne, growth of the prostate gland, and is integral in the development of male pattern baldness (androgenetic alopecia). Testosterone, on the other hand, is the classic “male” hormone, and is responsible for the changes seen at puberty: lowering of the voice, growth of the genitalia, an increase in muscle mass, and increased libido or sex drive. When testosterone is deficient, there may be decreased sex drive, erectile dysfunction, depression, lack of normal “drive” and ambition, and a loss of muscle mass. In other words, much of what DHT effects, we can do without! Testosterone, on the other hand, is extremely important. When men took the one milligram dose of Propecia, their DHT levels dropped by about two-thirds; on the other hand, testosterone levels were not only maintained in the normal range, but increased almost ten percent!
So the mechanism by which Propecia acts, unlike that of Rogaine, is well understood. Let’s look at what the studies and clinical trials showed about its effectiveness. 1,553 men, ages 18 to 41, with Norwood Class II Vertex, III Vertex, IV or V balding patterns (which are mild to moderate; the Class VI and VII are the most severe patterns) were given Propecia. At two years, 83% of those taking Propecia either grew more hair or at least lost no more. However, this effect was much more noticeable in the crown area than in the frontal or hairline zone. Also, the hairs that did grow in were longer and thicker, or more like terminal hairs, in contrast to the finer, shorter hair seen with the use of Rogaine.
Side effects seen were minimal in number. They included different types of sexual dysfunction (decreased sex drive, erectile dysfunction, decreased semen volume) at a total incidence of 3.8%. However, the group that received the placebo (sugar pill) had an incidence of 2.1%, which is not a large difference at all. Furthermore, these sexual side effects went away in all the men who stopped the medication, and in almost two-thirds of those who continued the medication!
6 to 12 months are required before any increase in hair is apparent; any sexual side effects would have occurred well before that time, so there is not a problem of losing hair that was gained on the medication when one stops taking it. Also, remember that if a person stops either Propecia or Rogaine, any hair lost will be only that which was gained or maintained while on the drug, and not any other; in short, one returns to the state of balding one would have experienced had one never taken the drug at all.
Another interesting finding in patients on Propecia is that it causes an approximately one-third reduction in the level of prostate-specific antigen (PSA). PSA is used as a screening test for prostate cancer; it also may be elevated in men with enlargement of the prostate. There has been some concern that this might compromise prostate cancer screening, even though the decrease in PSA in fairly predictable. To be safe, however, men should let their primary physician know if they are taking Propecia, so that this blunting effect on PSA can be taken into account.
Propecia does not seem to grow hair in areas that are completely bald. Its effects are apparent only in areas of the scalp that are thinning, but where there is still some hair present. Therefore, the major benefit of the drug seems to be in its ability to slow down or halt hair loss, or regrow hair in parts of the scalp that are miniaturized. The long-term ability of Propecia to maintain one's hair is unknown. Effects usually peak around one year and then are stable in the second year or decrease very slightly.
As previously stated, the benefits will stop if the medication is discontinued. Over the 3-6 months following discontinuation of Propecia, the hair loss pattern will generally return its native state (that is, as if no medication had ever been used).
Although both Propecia and Rogaine are FDA approved as being safe and effective, this does not mean that all the long term effects are known. Even though the side effects are rare, we can see that the drugs’ actions are not entirely confined to the scalp. We now have three to four years of experience with Propecia; only over time will the full ramifications of either of these agents be fully evident.
Many hair transplant surgeons find Propecia to be an excellent adjunctive medication, for several reasons: 1) Propecia works best in younger men; some of them may not be hair transplant candidates yet. 2) the medication works better in the crown area, and often the crown requires more surgically harvested donor hair than may be available. 3) Propecia is less effective in the front. Hair transplantation has its greatest impact on the hairline and in the frontal area. 4) If Propecia continues to slow or halt hair loss in the crown area, surgeons may be able to create greater density in areas such as the front, which will have a greater cosmetic effect, while sparing the all-important donor hair for the future.
While not an actual hair growth or maintenance product, there is a newer post-operative product that we will mention, known as GraftCyte, which is manufactured by the ProCyte Corporation. This line of products contains copper peptides, which have been shown to help with wound healing. The company makes a shampoo and conditioner, that are often recommended after transplant surgery, as well as a spray for hydrating the graft sites, and prepared, foil-wrapped sets of copper peptide saturated gauzes designed to be used for the first three post-operative days. In addition, there is a gel to be placed on the donor incision in the back of the head. All of these interventions may lead to improved, more rapid healing.
There are also claims that using the GraftCyte products promotes the more rapid growth of the transplanted hair. This has yet to be proven in controlled trials, but many people chose to use these products for their healing properties, and hope that these unproven claims are true as well.
Surgical Treatments for Hair Loss
History of Hair Loss Surgery
As early as the 1930’s, Japanese physicians were successfully harvesting and grafting multiple and single hairs into other areas of the body, including the scalp, face, and pubic region. The reports of these procedures were written in Japanese; this, together with the onset of World War Two, insured that the Western world remained in the dark until the late 1950’s.
In 1959, New York dermatologist Norman Orentreich reported hair-bearing scalp autografts (from the same person) that were successfully transplanted from the back of the head to the balding front and top. Thus the concept of “donor dominance” was introduced, and the discipline of hair restoration surgery in the West was born.
Donor dominance is the central functional principle of hair transplant surgery. What this means is this: if one harvests hair follicles from the “permanent zone” of the scalp, and transplants it to the balding areas, the donor hair characteristics will predominate. In other words, since this donor hair is genetically programmed not to respond to the male hormone DHT by becoming miniaturized, it will continue to grow and thrive even though its location is now in a balding “zone”.
Evolving Aesthetics of Hair Transplantation
For the first 20 to 25 years of hair transplantation, 3-4mm (millimeter) round, “plug” grafts were the standard units generally placed in balding areas. These were felt to be the optimal size grafts in terms of density (hairs per square mm) and in terms of blood flow (nourishment) to the tissues of the graft. In other words, these grafts, with 12 to 20 hairs each, could achieve high density in the recipient (balding) area; also, bigger grafts would be easier to move, but re-establishing their blood flow, especially toward the center of the grafts, would be tricky. Later, this was found to be a problem even with these standard grafts, and sometimes the hairs in the very center of the graft would die, leading to the appearance of a hole in the middle, hence the term “donutting”.
Other cosmetic problems were soon recognized. Often, a raised area at the base of the graft led to the aptly named “cobblestoning” effect. Probably the most widely recognized negative effect is the so-called “doll’s hair” “toothbrush” or “cornrow” appearance. This results from a dense, round graft set in the midst of bald scalp; the effect is worsened by the fact that, as the graft heals in place, scarring causes it to contract. This increases the density (compresses the hairs into a bundle) even more, to a level not found anywhere on the head, therefore appearing unnatural. When these round grafts were placed at the frontal hairline, they often appeared as an inhumanly straight, regular row, which is not the way hairs grow in nature. Furthermore, if the patient’s balding progressed, these grafts stood out even more, to the point of becoming a cosmetic nightmare. Also, if the hair behind the grafts was lost, there developed an unnatural look further back in the scalp; this appears as a posterior, or “rear” hairline.
In addition, the normal, natural direction of hair growth was not honored. Hair from the crown up to the front grows in a generally forward direction; there is a “whorl”, or circular effect at the crown, and at the temples the hair abruptly changes to a downward, and then backward, direction. Often the large grafts pointed up at right angles regardless of location, which added to the less than natural appearance, and could severely limit styling options.
From a logistical standpoint, grafting with standard plugs could be a nightmare. Usually, these were done in small sessions of 20 to 50 grafts at a time; then sessions were repeated after a period of time. This might require 4 or 5 sessions to “complete” the work; if financial, health, job, or other circumstances supervened, the work might not be finished, leaving the patient in an embarrassing state of incompleteness. Moreover, if baldness progressed, the rear or side margins of the plugs could then be seen by the casual observer.
Finally, using large, round grafts is an extremely inefficient use of the donor hair supply. Much hair is left in the scarred spaces between the circular holes in the donor area. The punch tool must be held perfectly parallel to the angle at which the hair emerges from the scalp; otherwise, many of the hair follicles at the edges of the graft will be transected, or cut in two. This destroys the hair, or, at the very least damages its ability to grow and thrive. Making the punch tools smaller failed to solve the problem the problem of transection; with a smaller graft, an even higher percentage of hairs per graft could be damaged. Likewise, when 4mm grafts were “quartered” or otherwise divided into smaller grafts, this required further trauma and manipulation with resultant follicular damage or destruction.
Many men were happy just to have hair again, and never complained about these cosmetic conundrums, or were aware of the technical limitations. However, certain creative surgeons begin to move toward a higher aesthetic ideal. In the early 1980’s, hair restoration specialists began utilizing minigrafts and micrografts. We define minigrafts as containing 5-10 hairs, and being between 1 and 2.5mm in diameter. Micrografts are smaller still: 1 to 1.5mm, with 1 to 3 hairs. Follicular unit grafts are the naturally occurring growth units of hair, and will be discussed in great detail in subsequent sections.
What were the benefits of these smaller grafts? For one thing, they could be used to “soften” the hairline. The hairline is naturally a feathered, indistinct, and variable entity; it is not abrupt, extremely dense, or regular. Usually, the first row or two of the hairline are single hairs, a “transition zone” between the hairless forehead and the hair-covered scalp. Also, the line is not straight at all, but irregular. Placing these small grafts at the hairline, in front of the larger, round grafts, gave a more pleasing, natural look, especially with the hair swept back or diagonally to the side.
Despite this and other benefits of using mini- and micro-grafting techniques, there was still a major downside (and still is today, as some hair transplant surgeons stubbornly cling to the old but familiar ways). Minigrafts can still produce the artificially high, local density leading to the doll’s hair look; they have a tendency to appear “pluggy”. Also, grafting large areas with micrografts often can give a “see-through” or excessively thinned look. The reason for this is quite important to understand; although a 2 hair follicular unit and a 2 hair micrograft contain the same number of hairs, the devil is in the details; the major detail is in the way they are cut. Follicular units are dissected out intact, using a microscope, and thus have the minimal amount of tissue present to support the hairs. Conversely, micrografts are cut without regard for the follicular unit structure; a 2 or a 3 hair micrograft may contain hairs from as many as 2 or 3 separate follicular units! As such, they contain much more tissue than corresponding follicular units, require larger recipient incisions, or even holes, and cannot be placed as closely together. Healing takes longer with these excess tissue-containing grafts, and their larger incisions, and it may be that breaking up the fundamental unit of hair growth inhibits the very survival of the grafts themselves.
Plastic surgeons have developed methods of advancing hair-bearing “flaps” of tissue from one area of the scalp to another. For example, a strip of scalp from the non-bald temple might be freed up, and rotated forward to the bald frontal hairline. A small area of the flap is left attached in order to preserve the blood supply of the tissue. Unfortunately, sometimes the blood circulation is compromised, leading to tissue necrosis, or death of part of the flap. This can cause visible scarring, as well as loss of the hair (!) from that portion of the flap.
The benefit of flap procedures is that one has an instant “growth” of mature, full-length hair in the previously bald area. There is nothing subtle or gradual here! This may be a social liability if one desires privacy regarding the surgery.
This is major surgery, requiring a hospital operating room. Bleeding and infection are other possible complications. Also, there is a cosmetic downside. A hairline constructed with a flap is likely to be unnaturally straight and overly dense, unlike the natural “feathered” transition zone found in a natural or surgically well-constructed hairline. The inevitable scar at the leading edge of the flap may also be apparent to the observer. Also, there may be thinning or balding scalp behind the flap, which requires camouflage. Alterations from the normal direction of hair growth can appear nothing short of bizarre. Thus we see little benefit and abundant potential for negative outcomes with flap procedures.
These procedures are collectively known as alopecia reductions, baldness reductions, male pattern reductions, and by other names. The basic premise is, that by excising, or cutting out, a segment of bald scalp, the baldness is reduced. This provides an immediate and relatively dramatic improvement in the balding appearance, and the added benefit of less area needing to be grafted. This would limit the strain on the patient’s finite “donor reserves”, meaning the hair available from the permanent zone that can be harvested for grafting. This may seem intuitively obvious at first glance, but consider this: when scalp is removed from the crown area and the top of the head, the sides and back are pulled up in order to approximate the wound and suture it closed. The effect this can have on the donor hair in the back and sides of the head is to decrease the density of this hair.
Other problems that slowly became evident included the phenomenon of stretchback, whereby the natural elastic properties of the scalp skin overcame the tension element of the scalp reduction, and some or all of the benefit would be lost. Hair loss may be accelerated by scalp reductions, in the opinion of some hair surgeons; we definitely know that “shock loss”, or effluvium, can occur around the incision. Some of this shock loss hair may or may not grow back, largely depending on its state of miniaturization.
Scarring is one of the most significant complications seen after scalp reduction. There are a number of incisional patterns that surgeons use: the midline ellipse, Mercedes star, Z-plasty, and lazy-S. The end result of any of these will be a scar in the shape of the sutured wound. This scar may be more or less noticeable depending, in part, on whether there is continued balding in the area, or how closely adjacent to the scar dense hair is found. The fact of the matter is that the patient’s donor density and scalp laxity can be reduced by the procedure. These are two of the determinants of the amount of donor “reserves” remaining. If they are reduced enough, there may not be enough hair left to graft over the scar if it is, or becomes, obvious to the casual observer. This is a major cosmetic problem.
While scalp reductions are often done as series of two or three, some surgeons will substitute for the series by doing one large procedure. This is known as a scalp lift or hair lift. It requires general anesthesia, and essentially undermines the scalp down to the ears and down to the neck. Then, the loose scalp is pulled up, the balding area removed and the wound edges stitched together. It is also standard procedure to ligate, or tie off, the major arteries to the back of the head, called the occipital arteries. Usually, the occipital nerves are sacrificed in the bargain, leading to significant and long lasting scalp numbness.
There are also various types of scalp expanders, both inflatable and spring-type. Both types are surgically implanted, and are designed to stretch the scalp prior to the reduction surgery. Their effects are variable, and although some surgeons seem to do well with their use, many of the same potential drawbacks of scalp reductions may occur.
Two other well-known cosmetic deformities resulting merit mention here. One is the loss of normal hair direction, often manifesting as the “parting of the Red Sea” phenomenon. This occurs because when the scalp is pulled up from the sides, and then becomes situated on top of the head, its hair will still emerge at its native angle. In short, it may appear to stick out to the sides from the midline in an unnatural way, like the biblical parting of the Red Sea. Another is the “posterior slot” formation, which also occurs as the result of scalp reduction surgeries. This “slot” appears as vertical scar running down the crown of the head, with the adjacent hair angled out flatly. This is a very obvious deformity; there is a flap surgery designed just to correct this problem (!), but it is complex and not performed well by many surgeons.
We feel that scalp reduction procedures generally have a very high risk to benefit ratio. As such, we would rarely recommend these surgeries, except in certain selected patients with the ideal hair and scalp characteristics, of the optimal age, and who are highly motivated. With all other factors considered, properly performed follicular unit transplantation (FUT) can produce natural, undetectable results, without cosmetic deformity, in patients who are candidates for this procedure. In the next section, we will discuss, at length, FUT, why and how it is done, the rationale for, and history of, its development, and its potential drawbacks.
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