Risk Factors of Keloids: A Mini Review

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Citation: Shaheen AA. Risk Factors of Keloids: A Mini Review. Austin J Dermatolog. 2017; 4(2): 1074.
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Abstract
Keloid is a benign brous growth, which presents in scar tissue of
predisposed individuals. It is a result of irregular wound healing, but the exact
mechanism is unknown. However, it is possible that several factors such as
age of onset, sex, cause of scarring, blood groups, anatomical site, presence
of family history and number of injured sites (multiple/single) have an important
role in keloid formation and consequentially in predicting keloid’s behavior in
response to treatment and prognosis. In this mini review, we have demonstrated
these risk factors of keloids in detail.
Keywords: Keloids; Risk factors; Family history; Melanin; Blood groups;
Cause of scarring; Anatomical site; Multiple sites; Sex; Age of onset
Introduction
Keloid is a benign brous growth, presents in scar tissue of
predisposed individuals, extends beyond the borders of the original
wound, doesn’t usually regress spontaneously, and tends to recur
aer excision. It is a result of irregular wound healing following skin
insults (trauma, inammation, surgery, burns…etc.), but sometimes
occur spontaneously. Most keloids develop within 3 months of the
injury, but some may occur up to 1 year aer skin insults [1]. First
described in the Edward Smith papyrus in Egypt around 1700 BC [2].
Keloids appear as rm, mildly tender, boss elated tumors with a shiny
surface. In the Caucasian patient, keloids tend to be erythematous
and telangiectatic; they are oen hyperpigmented in darker-skinned
individuals. Keloids are oen pruritic and painful, in addition to
signicant eects of patient’s quality of life, both physically and
psychologically, especially in excessive scarring [3,4].
e main dierential diagnosis of keloid is hypertrophic scar,
also called pseudokeloid. Dierential diagnosis is important, since
treatment procedures dier between these two types of scar disorders.
Hypertrophic scars, which dened as raised scars that remained within
the boundaries of the original lesion, oen regressing spontaneously
aer the initial injury and rarely recurring aer surgical excision.
In contrast, a keloid scar is dened as a dermal lesion that spreads
beyond the margin of the original wound, continues to grow over
time, does not regress spontaneously and commonly recurring aer
excision [1].
e process by which keloid develops is poorly understood, but
it is known to be induced by skin insults in predisposed individuals.
ere are several theories of keloid etiology, most of them are related
to broblast dysfunction. Keloid broblasts, when compared with
broblasts isolated from a normal wound, have excessive deposition
of extracellular matrix components, especially collagen, bronectin,
elastin, proteoglycans. In addition, these cells have lower rates of
apoptosis [2,5].
Risk Factors of Keloids (Epidemiology and
Etiology)
Several factors play a signicant role in keloids formation. e
Mini Review
Risk Factors of Keloids: A Mini Review
Shaheen AA*
Department of Dermatology, Tishreen University, Syria
*Corresponding author: Abeer Ali Shaheen,
Department of dermatology, Tishreen University,
Lattakia, Syria
Received: May 17, 2017; Accepted: June 12, 2017;
Published: June 19, 2017
genetic predisposition is the most important factor; other factors are
blood groups, melanin, the anatomical site, the type of skin injury, the
age of onset, and sex [1].
Genetic predisposition
ere is a clear genetic component given the correlation with
family history, which supported by the following phenomena: (a)
some patients with keloids report a positive family history. 19.3%
of Syrian patients had a family history [1], 50% of Afro Caribbean
patients [6], and 36.4% of Nigerian patients [7]. (b) High occurrence
in identical twins [6,8,9]. (c) ere are higher predisposition in Blacks,
Hispanics and Asians, less frequently in Caucasians [6]. (d) Increased
incidence of keloids in patients with some genetic syndromes like
Turner syndrome, Opitz-Kaveggia syndrome, Rubinstein Taybi
syndrome and Ehlers Danlos syndrome [10].
Proposed inheritance patterns include autosomal recessive,
autosomal dominant with incomplete penetrance, and variable
expression [8,11]. Several genes are considered responsible for keloid
disease, but no single gene mutation has thus far been found to be
responsible [12].
(a) Genome wide association study in Japanese population
has shown that four SNP (Single Nucleotide Polymorphism) loci
in three chromosomal regions (1q41, 3q22.3-23 and 15q21.3)
exhibit signicant associations with keloids [13]. (b) Marneros
and colleagues studied two families with an autosomal dominant
inheritance pattern of keloids (Japanese family and African American
one). ey identied linkage to chromosome 2q23 (maximal two-
point LOD score of 3.01) for the Japanese family. e African-
American family showed evidence for a keloid susceptibility locus
on chromosome 7p11 (maximal two-point LOD score of 3.16) [14].
(c) Brown and colleagues found a genetic association between HLA-
DRB1*15 statuses and the risk of developing keloid scarring in white
individuals [15]. (d) Also, carriers of HLA-DQA1*0104, DQB1*0501
and DQB1*0503 have been reported to be have an increased risk of
developing keloid scarring [3].
ere is importance of the cause and anatomical site in the added
heredity of keloids. 76% of patients with family history have keloids
located in the same anatomical sites of the relative, and 66% of them

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have keloids caused by the same cause [1]. Also, there is predisposition
to heredity spontaneous keloids, which usually appears in the second
decade, presternal and shoulder keloids [1]. In addition, family
history is strongly associated with the formation of keloid scars in
multiple sites as opposed to a single anatomical site [6].
Blood groups
People with blood group A have high probability to develop
keloids compared with other blood groups, that may be partly
explained by the association between the eect of red cell antigens
A (which present on the membrane surface of red blood cells and
certain epithelial cells) and other factors in these patients [1,9]. A
study by Shaheen [1] revealed association between spontaneous
keloids and blood group A (p = 0.01), which conrms the eect of red
cell antigens A in development of keloids. (is nding has not been
previously reported).
Melanin
ere is a relationship between keloid formation and skin color,
as supported by the following phenomena: (a) Colored skin people
such as the Negroid and Mongoloid races have a greater tendency to
suer from keloid compared to the Whites (the Caucasian race). e
comparative ratio between Blacks and Whites who suer from keloid
varies extensively, ranging from 5 up to 18.7 to one. On the other
side, evidently keloid is not found among albino which is a condition
where there is absent or minimal melanin pigment [5,6,16-18]. (b)
e incidence of pathological scarring varies across dierent parts
of the body even in the same individual; for example, fewer keloids
develop in the palm and thenar eminence, where melanocytes are
less common [17,19]. (c) Adolescents and pregnant women, who are
subjected to increased hormone secretion and skin pigmentation, are
more susceptible to developing keloids [17]. Based on these facts, it
becomes apparent that the incidence of keloid is strongly related to
skin color. Melanin is the most important pigment which determines
variations in skin color of the various races in the world [2,20].
e relationship between melanin and keloid formation have been
assumed by several theories: (a) During wound healing, melanocytes
from the stratum basal contact or interact with broblasts from the
dermal layers aer the basal membrane is damaged, which in turn
facilitates broblast proliferation and the secretion and deposition of
collagen [2]. (b) High levels of melanin cause decreasing of histologic
PH, which inhibit collagenase, that disrupts collagen degradation
process [20].
Causes of keloids (Type of skin injury)
Keloids may develop following any skin injury like non-
inammatory conditions such as burn, trauma, surgery, piercings,
or inammatory skin conditions such as acne vulgaris, folliculitis,
varicella infection, or vaccinations (particularly BCG vaccination)
[3,19], but not all such insults lead to a keloid scar even in the
susceptible individuals [6]. is means all types of skin injuries could
cause keloids, but each patient is aected by specic type of injuries.
at indicate to the role of type of skin injury in keloid formation,
which supported by the higher prevalence of single keloid more than
multiple keloids, although the patient is exposed to other injuries that
may cause keloid. On other hand, there are very few patients have
keloids caused by two dierent causes [21].
e most common cause of keloid diers according to conditions
of study’s society. Syrian [1] and Iranian studies [22] found that
keloids could follow any form of skin injury, but burns were the most
common. Bayat [6] found that laceration was the most common cause
in Afro Caribbean patients. However, the occurrence of a keloid or
hypertrophic scar following BCG vaccination is not uncommon
and is likely more to the inammatory nature of the injection
response rather than the size of the wound [19]. Causes have almost
coordinated distribution in males and females, but males have higher
predisposition to develop acne keloids compared to female, because
only males have acne keloidalis nuchae, and the severity of acne is
higher in them [1].
Spontaneous keloid is a rare condition, and it is controversial
whether it is in fact spontaneous. e scar tissue may form aer an
insignicant inammatory reaction or injury which the patient has
no recollection of. Syrian study [1] found 13.4% of spontaneous
keloids, which was similar to Togo study 13.13% [21], but lesser
than an Iraqi one 34% [23]. As we said before, some patients have
hereditary of spontaneous keloids, while others have association with
blood group A [1]. ere is conrmed evidence of the association
between spontaneous keloid formation and dierent diseases such
as Dubowitz syndrome, Rubenstein-Taybi syndrome, and Noonan
syndrome. In addition, Spontaneous keloid has been reported in
siblings and in people with allergic diseases [24].
ere are very few patients have keloids caused by two dierent
causes [1]. ey are only 2.32% of patients in Syrian study [1], 83.3% of
them had surgical keloids, so we have to be careful when performing
surgery for a patient who had a previous keloid. On other hand, this
percentage is higher in dark skin patients 15.9% [21], maybe because
developing keloid is more common in Blacks than in Whites.
Keloids could follow any skin insults, but there is association
between anatomical sites and specic injuries. Shaheen [1] found
that burn was the most common cause of keloid formation in
uncovered sites (face (35%), neck (50%), upper limbs (44.29%, lower
limbs (66.66%), and chest wall (27.59%)),) and less aected sites
(lower back (37.5%), button (50%), genitalia (50%), palm and sole
(66.66%)), which disagree partly with the Japanese study, found that
trauma was the most common cause of extremities keloids [25]. Ear
piercing is the most common cause for earlobe keloid [1,6,25]. Acne
is the most common cause for scalp keloids [1,6]. More than quarter
of shoulder keloids were caused by acne [1,25]. e Syrian study [1]
found that Most sternum keloids were spontaneous (35.82%), or
followed surgery (37,13%), while most sternum keloids were caused
by trauma in Jamaican study [6], or acne in Japanese study [25]. At
last, abdominal keloids followed by surgery in several study, more
than half of abdominal keloids followed surgery in the Syrian study
[1], while all abdominal keloids followed surgery in the Japanese
study [25].
Anatomical site
Several studies indicated to the role of anatomical site in keloid
formation, which supported by the following phenomena: (a)
Genetically susceptible individuals form keloids aer wounding
but not at every body site [6]. (b) Generally keloids tend to occur
on highly mobile sites with high tension such as shoulders, neck,
and presternum [26,27]. (c) ere are familial patterns of keloid
distribution [11].

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Anterior chest, shoulders, earlobes, upper arms and cheeks have
a higher predilection for keloid formation. Eyelids, cornea, palms,
mucous membranes, genitalia and soles are generally less aected
[3]. e most common anatomical site for developing keloids diers
according to race, traditions and conditions of study’s society.
Shaheen [1] indicated that upper limb 20% followed by sternum
19.17% were the most common sites for developing keloids in Syrian
patients. Similarly, Abas Mouhari Toure [21] noted that sternum
28.95%, upper limb 15.8% and head 16.7% were the most common
sites in dark skin patients. Conversely, ear 23% was the most common
one in Bayat’s study [6]. On other hand, most of studies agree that
genitalia, buttock, palm and sole are the rarest sites for developing
keloids [1,6,7,21].
Few studies discussed the development of keloids in single versus
multiple anatomical sites and its correlation with patient’s clinical
feature and prognosis [1,6]. Shaheen [1] found that 19.3% of patients
had keloids in multiple anatomical sites, where upper limb was the
most common site for developing keloids in them 46%, and burn was
the most common cause 38.2%. Bayat [6] demonstrated that 42.2% of
patients had keloids in multiple anatomical sites, where earlobe was
the most common site in multiple 24% sites, and ear piercing was the
most common cause. Although all causes tend to develop keloids in
multiple sites, only burn and acne have association with developing
keloid in multiple sites in Syrian patients (p = 0.029) (p = 0.0002)
respectively, which means there is high probability to develop acne or
burn keloids in another anatomical site in a patient who had a previous
acne or burn keloid respectively, because both acne and burn could
aect multiple sites more than other causes, which is more located
[1]. Female sex, younger age at presentation and the presence of a
positive family history are associated with the development of keloid
scars in multiple anatomical sites in Afro Caribbean individuals [6].
A previous study reported that 1.93% of patients have keloids caused
by two dierent causes, and distributed on multiple anatomical sites.
is may be indicate that very few people have a high predisposition
to develop keloids, but this nding needs more research.
Keloids could develop at any anatomical sites, but there is
association between type of skin injury and specic anatomical sites.
Syrian study [1] found that 80% of spontaneous keloids were located
on sternum and shoulders, this agree partly with a previous study,
which demonstrated that sternum was the most common site for
spontaneous keloids [28]. Also, 45% of burn keloids were located on
extremities (lower and upper) in that study [1], while a Japanese study
found that all burn keloids were located on chest wall and lower limbs
[25]. About 40% of sharp wound keloids were located on upper limbs,
and 50% of surgical keloids were located on sternum and abdominal
wall [1,25]. Sternum and shoulder are the most common site for acne
keloids. Syrian study [1] found that about half of acne keloids were
located in these sites, while most acne keloids were located in these
sites in the Japanese study [25]. 37% of trauma keloids were located
on face and upper limb in Syrian patients [1], which agree partly with
the Japanese study [25], which found that most trauma keloids were
located on extremities (upper and lower).
Epidemiologic variances (sex and age)
Incidence of keloids is usually equal in females and males
[9,21,23,29], but sometime there is higher incidence in female [6,29]
(it could be related to the higher rate of earlobe piercing in females),
or in male (it could be related to acne keloidalis nuchae, especially
in Blacks) [7]. In general, both sexes develop keloids in the same
anatomical sites, and followed to the same injuries, but sometimes
there is preference for one gender to develop keloids in specic site,
following specic cause, at specic age. Males who are older than forty
could develop keloids more than females in the same age (as we will
discuss later). Also, males have higher predisposition to develop acne
and scalp keloids compared to female, because only males have acne
keloidalis nuchae, also, the severity of acne is higher in them [1]. As we
said before, Female sex is associated with the development of keloid
scars in multiple anatomical sites in Afro Caribbean individuals [6].
Although keloids could occur at any age, they are rare in rst
decade, because people in this decade are not stimulated by sexual
hormones (higher incidence of keloid formation during puberty)
[1,3,16]. Most likely to occur in second and third decades and tend
to decrease in older [1,6,9,17], which supported by the following
phenomena: (a) younger people may have a higher frequency of
trauma, their skin is more elastic than the skin of elderly people [29],
(b) they have higher level of sexual hormone than older people (Keloid
growth may also be stimulated by various hormones, as indicated
by some studies in which results have suggested a higher incidence
of keloid formation during puberty and pregnancy, with a decrease
in size aer menopause, that related to localized hyper androgen
metabolism which may play a causal or at least contributory role
in the pathogenesis of keloids, or elevated androgen receptor levels
exist in clinical active keloid tissue [30,31]) [1,3,16,19]. Also, younger
age is associated with the development of keloid scars in multiple
anatomical sites [6]. Each decade has preference to develop keloids
in specic site, following specic cause. Burn is the most common
cause for developing keloids in rst decade compared with other
decades, especially on upper and lower limbs. is is a logical result,
because most of burn accidents exist in younger children especially
on extremities [1]. Occurrence of acne keloids is higher in second
decade compared with other decades, because the peak in prevalence
and severity of acne occurs in second decade. High frequency of
sharp wound accidences and earlobe piercing in second decade
explain the higher incidence of these keloids in this decade [1]. Also,
development of scalp keloids is higher in second decade compared
with other decades, because most cases of acne keloidalis nuchae
occur in persons aged 14-25 years (most cases of scalp keloids are
caused by keloidalis nuchae) [1]. ere is absence of acne keloids in
fourth decade, because frequency of acne extremely decrease in this
decade [1]. At last, development of surgical keloids is higher in h,
sixth and seventh decades compared with other decades, especially on
sternum. ese results reect an increase of open heart surgeries in
older people, especially for males who are older than forty compared
to females in the same age [1].
Note: e above risk factors are unmodiable factors, but there
are modiable factors like delayed healing [32], and hypertension
[33].
Delayed healing
is usually occurs as a result of wound infection or if wound
edges are not apposed. is will lead to healing by second intention
as the defect lls gradually with granulation tissue and restoration of
epidermal continuity may take a considerable time. Healing by second

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intention usually results in prolonged healing, excessive brosis and
an ugly puckered scar as opposed to healing by rst intention which
occurs following the meticulous apposition of the edges of clean
incised skin. is leaves a narrow epidermal defect which can be
bridged easily resulting in a ne hairline scar. us healing by second
intention is more likely to develop keloids especially if healing time is
greater than three weeks [32].
Hypertension
ere is relationship between hypertension and development of
severe keloids. Blood pressure associated significantly and positively
with both keloid size and number (both p <0.0001). is association
may reflect the fact that hypertension damages blood vessels, thereby
increasing inflammation in local tissue [33].
Treatment
No single therapeutic modality is best for all keloids. e location,
size, and depth of the lesion; the age of the patient; and the past
response to treatment determine the type of therapy used. ere are
several options in keloid treatment [34].
Standard treatments
ese include occlusive dressings, compression therapy, and
intralesional corticosteroid injections. Occlusive dressings include
silicone gel sheets and dressings, nonsilicone occlusive sheets, and
cordran tape. ese measures have been used with varied success.
Antikeloidal eects appear to result from a combination of occlusion
and hydration, rather than from an eect of the silicone. Compression
therapy involves pressure, which has long been known to have
thinning eects on skin. Reduction in the cohesiveness of collagen
bers in pressure treated hypertrophic scars has been demonstrated
by electron microscopy. Cellular mechanoreceptors may have an
important role of compression therapy. Mechanoreceptors induce
apoptosis and are involved in the integrity of the extracellular matrix.
Corticosteroids, specically intralesional corticosteroid injections,
have been the mainstay of treatment. Corticosteroids reduce excessive
scarring by reducing collagen synthesis, and reducing production of
inammatory mediators and broblast proliferation during wound
healing. e most commonly used corticosteroid is Triamcinolone
Acetonide (TAC) in concentrations of 10-40mg/mL administered
intralesionally at four to six week intervals. Intralesional steroid
therapy as a single modality and as an adjunct to excision has been
shown to be ecacious in various studies.
Cryotherapy
Cryosurgical media like liquid nitrogen aects the
microvasculature and causes cell damage via intracellular crystals,
leading to tissue anoxia. Generally, 1, 2, or 3 freeze-thaw cycles lasting
10-30 seconds each are used for the desired eect. Treatment may
need to be repeated every 20-30 days.
Excision
Decreased recurrence rates have been reported with excision
in combination with other postoperative modalities, such as
radiotherapy, injected IFN, or corticosteroid therapy.
Radiotherapy
Radiation destroys broblasts in the wound, prevents
neovascularization, which ultimately leads to a decreased production
of collagen.
Laser therapy
Ablative lasers (carbon dioxide 10,600nm, Erbium: Yttrium
Aluminum Garnet Laser Er: YAG 1064nm, and Argon 488-nm
laser). Nonablative lasers (Pulsed-dye laser 585nm): it provides
photothermolysis, resulting in microvascular thrombosis. e PDL
remains the laser treatment of choice for keloids hypertrophic scars.
Intralesional\topical apply of following drugs: IFN injections,
5-Fluorouracil, Doxorubicin (Adriamycin), Bleomycin, Verapamil,
Retinoic acid, Imiquimod 5% cream, Tamoxifen, Tacrolimus, and
Botulinum Toxin A.
Other promising therapies
e antiangiogenic factors, including the Vascular Endothelial
Growth Factor (VEGF) inhibitors (e.g. Bevacizumab). Phototherapy
(Photodynamic erapy - PDT), UVA-1 therapy, narrow band UVB
therapy. Tumor Necrosis Factor (TNF) alpha inhibitor (etanercept).
Recombinant Human Interleukin (rhIL-10) which are directed at
decreasing collagen synthesis [34].
Conclusion
It is possible that several factors have an important role in keloid
formation and consequentially in predicting a keloid’s behavior in
response to treatment and prognosis. e genetic predisposition is
the most important factor, but no single gene mutation has thus far
been found to be responsible. People with blood group A have high
probability to develop keloids compared with other blood groups.
ere is a relationship between keloid formation and skin color,
Blacks have a greater tendency to suer from keloid compared to the
Whites. All types of skin injuries could cause keloids, but each patient
is aected by specic type of injuries, which indicate to the role of type
of skin injury in keloid formation. Genetically susceptible individuals
form keloids aer wounding but not at every body site, which indicate
to the role of anatomical site in keloid formation. ere is importance
of the cause and anatomical site in the heredity of keloids. Burn, acne,
female sex, younger age at presentation and the presence of a positive
family history are associated with the development of keloid scars
in multiple anatomical sites. Males who are older than forty could
develop keloids more than females in the same age. Also, males have
higher predisposition to develop acne and scalp keloids compared to
female. Although keloids could occur at any age, they are rare in rst
decade, most likely to occur in second and third decades and tend to
decrease in older. ere are modiable factors like delayed healing,
and hypertension.
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Citation: Shaheen AA. Risk Factors of Keloids: A Mini Review. Austin J Dermatolog. 2017; 4(2): 1074.
Austin J Dermatolog - Volume 4 Issue 2 - 2017
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