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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_537_Библиотеки_им_академика_М_И_Перельмана
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administration, and provide equitable healthcare for marginalized patients
throughout the rest of her career.
Emre Tokgöz completed two Ph.D. degrees, one in Mathematics and
another one in Industrial Engineering, at the University of Oklahoma along
with a master’s degree in Computer Science and two master’s degrees in
Mathematics. Due to his interest in biomedical engineering applications of
mathematics and engineering, he pursued an online biomedical engineering
master’s degree for professionals at Johns Hopkins University. His other
research interests include nonlinear optimization, game theory,
deep/machine learning, financial engineering, facility allocation problems,
vehicle routing problems, systems’ design and improvement, network
theory and analysis, inventory systems, and Riemannian geometry.
1 Introduction
In recent years, there has been rapid growth in the field of plastic surgery,
especially for nonsurgical aesthetic procedures. Advancements in the field
have allowed for improvement in reduction of age-related changes and
patient-desired enhancements with minimally invasive techniques. Recent
developments allow patients to achieve similar results while reducing risks
associated with more invasive surgery. Combined treatments, such as use of
neuromodulators in conjunction with injectable fillers, are well utilized to
target multiple aspects of aging. Nonsurgical procedures can also be useful
in enhancing the results of cosmetic plastic surgery when the invasive
technique is not able to fulfill the patient’s goals. The collaboration of
medicine and technology aims to provide patients with optimal results and
minimal risks, as the efficiency and precision of targeted therapies continue
to increase. The structure of the outcomes we present in this work is similar
to those presented in [248–282].
2 Hairline Rejuvenation
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The overall shape of the hairline in both men and women plays an
important role in balancing the aesthetic appearance of the upper face [1].
Male hair loss tends to occur in an M-shape, with losses around the
frontotemporal region of the face. Some women experience similar patterns
of hair loss, potentially inducing an undesirable masculine appearance [2].
With aging, hair loss and receding hairline can create the appearance of a
larger forehead. The three main options to surgically address the frontal
hairline are follicular unit transplantation (FUT), follicular unit extraction
(FUE), and hairline-lowering surgery (HLS) [3]. Hairline-lowering surgery
can help to reduce this appearance, although some patients wish to avoid
the resultant hairline scarring [4].
Hair transplantation surgery is well utilized to correct receding or
unaesthetic hairlines. Otherwise known as follicular transplantation,
surgeons can harvest follicles of hair from the same patient and transplant
them near the hairline. While there are additional considerations to maintain
a natural appearance, this approach minimizes scarring and effectively
changes the shape of the hairline while inducing the appearance of a smaller
forehead [5].
The more invasive surgical approaches are utilized after the nonsurgical
modalities have been attempted, as these typically incur less risk to patients.
The nonsurgical approaches discussed in this section include
pharmaceutical treatments and minimally invasive aesthetic treatments.
2.1 Review of Relevant Anatomy
Hair grows outward from the scalp as a part of a follicular unit, which is a
partially visible structure containing visible terminal hair follicles, vellus
follicles, arrector pili muscles, sebaceous glands, adipose tissue, deeper
sweat glands (eccrine coils) and neurovascular networks [6–8]. The number
of terminal hair follicles in each unit is a measure of follicular unit (FU)
density, typically ranging between 1 and 4 [9]. This varies across differing
racial demographics, with lower measured FU density in Asian and black
individuals (154–162 and 148–160 hairs/cm2 respectively) compared to
Caucasians (214–230 hairs/cm2) [10].
Several different cells are found in the terminal follicles, including stem
cells, mesenchymal cells, and immunocytes (macrophages, T cells, mast
cells) [11, 12]. The mesenchymal cells originate from the dermal sheath and
papilla, and stem cells are housed in the bulge of the follicle. This bulge is
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located about 1–2 cm below the skin [13]. The anatomy of hair follicles and
a microscopic view are shown in Fig. 1.
Fig. 1 The image illustrates the microscopic anatomy of the hair shaft and outer root in the sagittal
(a) and transverse (b) planes [14]
2.2 Pathophysiology of Pattern Hair Loss
There are several genes thought to contribute to male and female hair loss
over time, and pattern hair loss is a polygenic condition. While there is a
great deal of variation on an individual basis, each gender is subject to
specific identifiable patterns of hair loss. In both genders, these changes can
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occur shortly after puberty, beginning with initial minimal loss of terminal
hair follicles and progressing gradually over time [15].
The increase of androgens after onset of puberty is a trigger for the
development of hair loss in male individuals in sensitive areas of the body.
These include the scalp (vertex and frontal), axilla, pubis, and beard, as well
as the extremities. Testosterone is converted to dihydrotestosterone (DHT)
with the enzyme 5-alpha reductase, and DHT plays a role in normal hair
growth and development. Increases in DHT and 5-alpha reductase have
been previously linked to male-pattern hair loss. On the other hand,
individuals with deficiencies of the enzyme 5-alpha reductase are not
expected to experience similar patterns of hair loss [16, 17]. Variable onset
of male pattern hair loss is attributed to genetic variations of the androgen
receptor (AR) gene [18].
In general, men tend to experience initial hair losses in the central and
temporal scalp, forming an M-shaped region of receding terminal hair
follicles. The level and severity of the loss are not identical in all
individuals, and there is documented variation in location and pacing [15].
The variations of male pattern hair loss are shown in Fig. 2.
Fig. 2 Male pattern hair loss, or androgenic alopecia, is generally classified based on the severity
and geographical area of hair loss [19]
The etiology of female-pattern hair loss is not as well understood. There
are previously documented cases of receding hairline in women with high
androgen levels, as well as women with complete androgen insensitivity
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syndrome [20, 21]. The AR gene is not implicated, as it is located in the X
chromosome and inactivated in women. Previous genome-wide studies of
women with allelic variants in aromatase genes, namely CYP19A1, have
been shown to predispose these individuals to female-pattern hair loss [18].
Generally, hair loss can occur as early as puberty in women but worsens in
severity and distribution after menopause. Compared with men, there is less
destruction to the overall shape of the hairline, but some do experience
temporal hairline reductions. Overall, the hair tends to become diffusely
thinner across the central scalp and along the middle part, lending to a
“Christmas tree” appearance [22, 23].
Figure 3a, b showcase the traditional “Christmas tree” appearance of
female hair loss and more diffuse, severe pattern loss in comparison.
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Fig. 3 (a) (Left) “Christmas tree” female hair loss pattern of varying severity [24]. (b) (Right)
Diffuse female pattern hair loss of varying severity [24]
2.3 Preoperative Patient Assessment
A thorough past medical history should be taken to assess for contributory
conditions prior to initiation of nonsurgical rejuvenation. Underlying
medical conditions can impact the acceleration, severity, and age of onset in
pattern hair loss. These include, but are not limited to:
Anemia or other nutritional deficiencies
Metabolic syndromes such as diabetes mellitus or thyroid disorders
Gynecological history: Polycystic ovarian syndrome (PCOS)
Management of such existing pathology should be prioritized before
patients undergo hairline rejuvenation [15].
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Certain medications have been associated with hair loss, and treatment
may not provide patients with adequate aesthetic results if these
medications are continued. These include:
Chemotherapy drugs (Cyclophosphamide/Cytoxan,
Doxorubicin/Adriamycin)
Antidepressants/antianxiety medication (Buproprion/Wellbutrin)
Anticoagulants (Warfarin/Coumadin, Heparin)
Antiepiletics (Depakote, Keppra)
Beta blockers for hypertension treatment (Propanolol, Metroprolol)
Hyperthyroidism pharmaceuticals (Methimazole/Tapazole)
Gout treatments (Allopurinol/Zyloprim)
In most cases, stopping pharmaceutical treatment will allow for normal
or semi-normal hair regrowth. Some medications are necessary to maintain
the overall physical health of an individual and may contraindicate
rejuvenation [25–27].
A thorough physical examination should be performed to confirm a
diagnosis of uncomplicated pattern hair loss and rule out any
contraindicatory conditions. The initial visual assessment examines the
nails and scalp, in addition to the quality and density of terminal hair shafts
and follicles. Normal pattern hair loss in men presents with thinning and
receding hair near the vertex and frontal scalp, while women tend to have
greater losses on the midfrontal scalp (described above in further detail).
The Ludwig scale, among others, is used to grade the severity of femalepattern hair loss, and the Norwood scale is used for men [15, 28].
If any inflammation/redness, flaking skin, or scarring is visible on the
underlying cutaneous skin, this indicates additional testing to rule out
dermatological conditions [15]. Seborrheic dermatitis is often comorbid to
pattern hair loss and results from increased circulating androgens and
resultant increases in oil production [29]. Abnormal nail appearance (e.g.,
ridges or reduced integrity) points away from typical pattern hair loss and
may be indicative of autoimmune or drug-induced hair loss [30].
Additional diagnostic maneuvers can help to identify active hair loss,
which is usually not associated with typical pattern hair loss (unless it is
performed early in the process). With the hair pull test, tension is applied to
50–60 hairs. If at least 6 hairs are easily removed, this can be indicative of
atypical active hair loss and points away from late pattern hair loss [31].
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Using a dermatoscope gives the surgeon a closer look at the hair follicles
and surrounding scalp tissue. Key findings to confirm a diagnosis of pattern
hair loss include lack of scarring, variation in hair shaft diameter,
pigmentation of adjacent follicular skin, and smaller scattered areas with no
follicles present [30]. A biopsy of the scalp is usually not necessary unless
other dermatological conditions are suspected [32] (Fig. 4).
Fig. 4 A patient with alopecia areata is shown in the figure above, which is one of many disorders
leading to irregular hair loss. When a patient’s presentation is inconsistent with normal pattern hair
loss, additional testing is indicated prior to surgical consideration [33]
Due to the variation in its presentation, there are other differential
diagnoses that can present similarly to typical male/female pattern hair loss.
These include telogen effluvium, traction alopecia, alopecia areata, central
centrifugal cicatricial alopecia, traction alopecia, trichotillomania, lichen
planopilaris, and frontal fibrosing alopecia [34, 35].
2.4 Nonsurgical Modalities
2.4.1 Pharmaceutical Treatments
Individuals with nutritional deficiencies such as anemia would benefit from
iron supplementation and should first address the primary issue for hair loss
before attempting pharmaceutical rejuvenation [33]. Therapy to treat
hyperandrogenism (which is a common cause of polycystic ovarian
syndrome) includes hormonal birth control and anti-androgen
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pharmaceuticals, although the latter is not approved by the U.S. Food and
Drug Administration and can impact future pregnancies [36].
It is recommended that patients attempt nonsurgical hairline
rejuvenation prior to more invasive follicular transplantation. Medications
commonly used include minoxidil (indicated for female and male pattern
hair loss) and finasteride (male pattern hair loss) [15].
Minoxidil was originally designed to reduce hypertension, and it may
still be used today for this indication. It can be well utilized to encourage
hair growth and prevent additional loss in both men and women. Minoxidil
is better known by its brand name Rogaine and is available as a topical
solution or foam with varying concentrations (2–5%). Some patients prefer
to use the foam, as they find it less irritating and easier to apply throughout
the scalp. This medication is FDA approved and is considered relatively
safe, as it is unable to cross the blood–brain barrier and 95% is shown to be
eliminated from the body within 4days [37, 38].
The active ingredient (minoxidil) is converted to a salt form (minoxidil
sulfate) by enzymes on the scalp (namely sulfotransferase). Minoxidil
sulfate promotes active hair growth of telogen (dormant) hair follicles by
inducing entry into the anagen (growth) phase. Patients are advised to wait
at least 8weeks before assessing the efficacy of Minoxidil, as it may take
some time for improvements in hair thickness and growth to develop [39].
In male hair rejuvenation, higher doses of minoxidil are more effective
when assessed from the patient’s perspective. In contrast, there are no
significant self-perceived differences in the improvement of female pattern
hair loss with lower/higher doses. Common side effects include temporary
shedding, excessive hair growth (near the hairline or on the body), and
dermatitis. These effects are more prevalent with higher concentrations of
minoxidil (5% compared with 2%) [40, 41].
Finasteride is the other FDA-approved medication for men, well utilized
for reduction of hair loss and regrowth. This formulation is effective in
increasing the hair density (higher coverage and hair count) as well as hair
thickness. Men are instructed to take a 1–5 mg dosage orally, once daily
[41, 42]. While it has not received FDA approval for women (and is not
typically indicated), there are some documented improvements in women
with hyperandrogenemia with higher doses [43]. The active ingredient in
this medication (finasteride) is a competitive inhibitor of 5-alpha reductase,
preventing the conversion of testosterone to DHT. The overall reduction of
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