Skin tags Cutaneous angiofibroma (Fibrous papule of the face, Adenoma sebaceum , Acral fibrokeratoma, Pearly penile papules-PPP) Keloids and hypertrophic scars

1. FIBROUS AND FIBROHISTIOCYTIC
PROLIFERATIONS OF THE SKIN P.I
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3. CLASSIFICATION OF FIBROUS AND
FIBROHISTIOCYTIC PROLIFERATIONS
OF THE SKIN
1. Skin tags
2. Cutaneous angiofibroma
3. Dermatofibroma
4. Dermatomyofibroma
5. Superficial acral fibromyxoma
6. Sclerotic fibroma of the skin
7. Pleomorphic fibroma of the skin

4. CLASSIFICATION OF FIBROUS AND
FIBROHISTIOCYTIC PROLIFERATIONS
OF THE SKIN
8. Nodular fasciitis
9. Multinucleate cell angiohistiocytoma
10. Epithelioid fibrous histiocytoma
11. Connective tissue nevus
12. Infantile digital fibroma
13. Infantile myofibromatosis
14. Calcifying aponeurotic fibroma
15. Keloids and hypertrophic scars

5. CLASSIFICATION OF FIBROUS AND
FIBROHISTIOCYTIC PROLIFERATIONS
OF THE SKIN
16. Fibrous hamartoma of infancy
17. Fibromatoses
18. Plexiform fibrohistiocytic tumor
19. Atypical fibroxanthoma
20. Dermatofibrosarcoma protuberans
21. Giant cell fibroblastoma
22. Fibrosarcoma
23. Epithelioid sarcoma

6. SKIN TAGS

10. Multiple skin tags in the axilla

18. OVERVIEW
Skin tags are very COMMON
BENIGN SOFT fleshy
FIBROVASCULAR SKIN-COLORED
to PINK or occasionally
HYPERPIGMENTED,
PEDUNCULATED papular tumors.
Up to 50% of all individuals have
at least ONE SKIN TAG.
SKIN TAGS

19. OVERVIEW
THEY ARE ALSO DESCRIBED AS:
ACROCHORDONS
PAPILLOMAS
FIBROEPITHELIAL POLYPS
SOFT FIBROMAS
SKIN TAGS

20. ETIOLOGY
It is NOT KNOWN what causes skin
tags. However, the following factors
may play a role:
1. FRICTION
2.  GROWTH FACTORS,
particularly during pregnancy
or in acromegaly.
3. INSULIN RESISTANCE.
4. ?HPV
SKIN TAGS

21. CLINICAL FEATURES
Acquired THROUGHOUT LIFE
and INCREASE in FREQUENCY
with AGE in both sexes.
Range in size from 1MM to 5CM.
Sites of predilection SKIN FOLDS:
neck, axilla, groin, inframammary
region & eyelids.
SKIN TAGS

22. CLINICAL FEATURES
They have a SMOOTH or
FOLDED surface.
Can become IRRITATED or
INFARCTED.
They tend to be MORE
NUMEROUS in OBESE persons
and in those with TYPE 2
DIABETES MELLITUS.
SKIN TAGS

27. HISTOPATHOLOGY
Benign FIBROVASCULAR tumors
due to NORMAL EPIDERMIS or
EPIDERMAL HYPERPLASIA
overlying a dermal stalk.
SKIN TAGS

28. HISTOPATHOLOGY
A CORE of DERMIS made up of
loosely arranged COLLAGEN
FIBERS and BLOOD VESSELS
and/or SUBCUTANEOUS FATTY
TISSUE.
SKIN TAGS

29. TREATMENT
Skin tags are benign & can be
removed only for COSMETIC
REASONS.
SKIN TAGS

30. TREATMENT
Options include:
1. CRYOTHERAPY
2. SURGICAL EXCISION (often
snipping with scissors)
3. ELECTROSURGERY
4. LASER e.g. CO2 laser
SKIN TAGS

32. Electrosurgery and snipping with scissors

34. Carbon dioxide laser removal

36. ANGIOFIBROMAS

38. Fibrous papule of the nose - smooth, dome-shaped, skin-
colored papule

44. Fibrous papule of the face

45. Fibrous papule of the face

51. Koenen’s tumor

54. Acral fibrokeratoma - light pink exophytic papule arising
from the dorsal surface of the finger

55. Acquired digital fibrokeratoma- Slightly raised skin encircling
the base of an acquired digital fibrokeratoma, creating a moat

57. Pearly penile papules - Multiple small white papules along the
corona of the glans penis. Note the multilayered distribution.

64. OVERVIEW
SINGLE or MULTIPLE SMALL,
RED, or SKIN-COLORED PAPULES.
 DERMAL VESSELS with
surrounding FIBROSIS.
Several conditions related.
ANGIOFIBROMAS

65. CLINICAL TYPES
1. FIBROUS PAPULE OF THE FACE
2. ADENOMA SEBACEUM
3. ACRAL FIBROKERATOMA
4. PEARLY PENILE PAPULES (PPP)
ANGIOFIBROMAS

66. OVERVIEW
RELATIVELY COMMON
CLINICALLY INDISTINCT
SOLITARY, FIRM, SHINY papule;
mostly on the NOSE less
commonly on other areas of the
FACE.
The exact reason is UNKNOWN.
FIBROUS PAPULE
OF THE FACE
1

67. CLINICAL FEATURES
Usually ASYMPTOMATIC
Develops during LATE
ADOLESCENCE or EARLY ADULT
LIFE on the nose, or less often,
elsewhere on the face esp. the
lips.
More SKIN COLORED than RED.
FIBROUS PAPULE
OF THE FACE

68. CLINICAL FEATURES
It is a firm DOME SHAPED SHINY
lesion usually only a FEW MMS in
size, sometimes bearing a central
hair. It is persists UNCHANGED
lifelong.
Occasionally, lesions are SESSILE,
POLYPOID, or PAPILLOMATOUS.
FIBROUS PAPULE
OF THE FACE

70. Diffuse reddish colour and the pink or whitish colour in the
lesion representing fibrosis

71. DDx
1. SMALL BASAL CELL
CARCINOMA
2. PYOGENIC GRANULOMA
3. INTRADERMAL MELANOCYTIC
NEVUS
4. ADNEXAL TUMORS.
FIBROUS PAPULE
OF THE FACE

72. Histopathology of a fibrous papule - focal fibrosis &
vascular proliferation in the upper dermis

76. HISTOPATHOLOGY
Well-circumscribed SLIGHTLY
RAISED upper dermal lesion
composed of: Proliferation of
FIBROBLASTS  STELLATE,
SPINDLE cells and/or
MULTINUCLEATED cells.
FIBROTIC hyalinized STROMA
composed mainly of COLLAGEN
bundles with DILATED BLD VVS.
FIBROUS PAPULE
OF THE FACE

77. HISTOPATHOLOGY
The EPIDERMIS is NORMAL,
ACANTHOSIS or SLIGHTLY
ATROPHIC and FLATTENED RETE
RIDGES.
Occasionally, a sparse
INFLAMMATORY CELL
INFILTRATE of lymphocytes is
present.
FIBROUS PAPULE
OF THE FACE

78. IMMUNOHISTOCHEMISTRY
The lesional cells stain for factor
XIIIa and sometimes CD34.
FIBROUS PAPULE
OF THE FACE

79. TREATMENT
Dose NOT require any
TREATMENT May be removed for
COSMETIC reasons.
If desired it may be removed by
EXCISION BIOPSY
SHAVE BIOPSY
ELECTROSURGERY
FIBROUS PAPULE
OF THE FACE

80. OVERVIEW
MULTIPLE FACIAL
ANGIOFIBROMAS IN TUBEROUS
SCLEROSIS.
ADENOMA
SEBACEUM
2

81. OVERVIEW
RARE benign SOLITARY, SKIN-
COLORED DOME-SHAPED or
TALL FINGERLIKE PROTRUSIONS
with a hyperkeratotic surface.
Often areas of TRAUMA or
SUBCLINICAL INJURY.
ACRAL
FIBROKERATOMA
3

82. VARIANTS
I. ACQUIRED DIGITAL
FIBROKERATOMA (ADFK).
II. ACQUIRED PERIUNGUAL
FIBROKERATOMA
III. SUBUNGUAL & PERIUNGUAL
FIBROMAS OF TUBEROUS
SCLEROSIS (KOENEN TUMORS)
they tend to be multi-lobulated
and involve several digits.
ACRAL
FIBROKERATOMA

83. CLINICAL FEATURES
ASYMPTOMATIC
PROTUBERANCE.
MIDDLE-AGED adults
Lesions occurred not only on the
FINGERS, but also on the
proximal HAND, TOES, SOLE.
ACRAL
FIBROKERATOMA

84. CLINICAL FEATURES
Usually not exceed 1.5 cm in height
or diameter SOLITARY, SKIN-
COLORED to PINK, CONE-
SHAPED, KERATOTIC PAPULE.
CHARACTERISTIC COLLARETTE of
SLIGHTLY RAISED skin that
ENCIRCLES the BASE of the
lesion creating a MOAT-LIKE
configuration.
ACRAL
FIBROKERATOMA

85. DDx
1. CORNS
2. CUTANEOUS HORN
3. INFANTILE DIGITAL
FIBROMATOSIS
4. PYOGENIC GRANULOMA
(Lobular Capillary Hemangioma)
5. SUPERNUMERARY DIGIT
6. WARTS, NONGENITAL
ACRAL
FIBROKERATOMA

86. Acquired digital fibrokeratoma

87. Massive orthokeratosis; core of thick collagen bundles
oriented in vertical axis; small vessels in dermal papillae; no
nerves, eccrine ducts, or cartilage

88. Domed-shaped papule with overlying hyperkeratosis. The dermal core is
composed of increased collagen bundles and blood vessels oriented along
the vertical axis of the lesion.

89. Close up showing the increased collagen bundles and
blood vessels oriented along the vertical axis of the lesion.

90. HISTOPATHOLOGY
HYPERKERATOSIS most
PRONOUNCED toward the
SUMMIT of the lesion.
ACANTHOSIS, with ELONGATION
of the RETE RIDGES or can be
slightly attenuated epidermis.
ACRAL
FIBROKERATOMA

91. HISTOPATHOLOGY
Most commonly consists of a DERMAL
CORE composed of THICK, closely
INTERTWINED COLLAGEN BUNDLES
that are often oriented along the
VERTICAL AXIS of the lesion.
Between the collagen bundles are
numerous CAPILLARIES, varying
numbers of FIBROBLASTS, and thin
ELASTIC fibers.
ACRAL
FIBROKERATOMA

92. TREATMENT
SIMPLE EXCISION is curative;
recurrence is rare.
ACRAL
FIBROKERATOMA

93. OVERVIEW
ASYMPTOMATIC, MULTIPLE
SMALL PEARLY-WHITE DOME-
SHAPED to FILIFORM PAPULES in
a GROUP or ROWS along the
SULCUS or CORONA of the
GLANS PENIS
CIRCUMFERENTIALLY.
PPP
4

94. OVERVIEW
They're NORMAL ANATOMIC
variant present in between 8%
and 43% of men.
More common in
UNCIRCUMCISED men.
Often, lesions cause GREAT
ANXIETY to patients until their
BENIGN NATURE is clarified.
PPP

95. CLINICAL FEATURES
1-3 ROWS of tiny, 1–3 MM
GLISTENING, FLESH-COLORED,
WHITE or LIGHT PINK papules.
PERSIST THROUGHOUT LIFE;
however, they GRADUALLY may
become less noticeable with
increased AGE.
PPP

96. DDx
1. GENITAL WARTS
2. MOLLUSCUM CONTAGIOSUM
3. ECTOPIC SEBACEOUS GLANDS
(FORDYCE SPOTS)
PPP

97. PPP- Papule with fibroblasts, rich vascularity, dense connective
tissue

98. HISTOPATHOLOGY
Variable number of THIN-
WALLED DILATED BLOOD
VESSELS in the dermis with a
proliferation of FIBROBLAST cells
which may be STELLATE or
MULTINUCLEATED.
CONCENTRIC FIBROSIS may also
be found around skin
APPENDAGE structures.
PPP

99. TREATMENT
REASSURANCE - No treatment is
needed. Any destructive modality may
be employed but SCARRING is a risk.
REMOVAL OPTIONS (To alleviate
anxiety);
CRYOTHERAPY
ELECTRODESICCATION & CURETTAGE
SURGICAL EXCISION
CO2 LASER
PPP

101. KELOIDS AND
HYPERTROPHIC SCARS

111. Clawlike outline of a keloid

114. Keloid Formation After Laser Tattoo Removal

116. Massive recurrent facial keloid

119. OVERVIEW
Keloid are FIRM to HARD,
SMOOTH, GROWTHS due to
SPONTANEOUS SCAR
FORMATION and much LARGER
than the ORIGINAL WOUND.
KELOID &
HYPERTROPHIC SCARS

120. OVERVIEW
Keloids may form on ANY PART of the
body, although the EARS, UPPER
CHEST & shoulders are especially
prone.
While most people never form keloids,
others develop them after MINOR
INJURIES, burns, insect bites and acne.
DARK SKINNED people form keloids
more easily than Caucasians.
KELOID &
HYPERTROPHIC SCARS

121. WHAT ARE HYPERTROPHIC
SCARS?
As wounds heal, SCAR TISSUE
forms, which at first is often
ERYTHEMATOUS and somewhat
PROMINENT.
Over several MONTHS, a scar
usually becomes FLAT and PALE.
If there is a LOT of TENSION on a
healing wound, the healing area is
RATHER THICKER than USUAL. This
is known as a HYPERTROPHIC SCAR.
KELOID &
HYPERTROPHIC SCARS

122. WHAT ARE HYPERTROPHIC
SCARS?
Hypertrophic scars remain
LIMITED to the TRAUMATIZED
AREA.
Regress SPONTANEOUSLY within
12-24 months, although
regression may NOT necessarily
be COMPLETE.
KELOID &
HYPERTROPHIC SCARS

123. PREVALENCE
The prevalence has been reported
to be HIGHER in YOUNG FEMALES
than in young males, probably
reflecting the greater frequency of
EARLOBE PIERCING among females.
Keloids and hypertrophic scars
affect BOTH SEXES equally in OTHER
AGE GROUPS.
KELOID &
HYPERTROPHIC SCARS

124. ETIOLOGY
The EXACT MECHANISMS of keloid
and hypertrophic scar pathogenesis
continue to be an ENIGMA for
physicians and researchers alike.
The INCREASED PREVALENCE of
keloids paralleling increased
CUTANEOUS PIGMENTATION
suggests a GENETIC BASIS or, at
least, a genetic linkage.
KELOID &
HYPERTROPHIC SCARS

125. ETIOLOGY
TRAUMA TO THE SKIN, both physical
(e.g. earlobe piercing, surgery) and
pathological (e.g. acne, chickenpox),
is the primary cause of keloids.
THE PRESENCE of FOREIGN
MATERIAL, INFECTION, HEMATOMA,
or increased SKIN TENSION can also
lead to keloid or hypertrophic scar
formation in susceptible individuals.
KELOID &
HYPERTROPHIC SCARS

130. CLINICAL FEATURES
Keloids and hypertrophic scars do
NOT usually cause SYMPTOMS, but
they MAY be TENDER, PAINFUL, or
PRURITIC or they may cause a
burning sensation.
In addition to symptomatic relief,
COSMETIC CONCERN is the primary
reason patients seek medical
intervention.
KELOID &
HYPERTROPHIC SCARS

131. CLINICAL FEATURES
Keloids manifest as EXAGGERATED
GROWTHS of SCAR TISSUE, USUALLY
in areas of PREVIOUS TRAUMA.
Keloids extend BEYOND the areas of
trauma, PROJECTING ABOVE the
LEVEL of the SURROUNDING SKIN,
but they rarely extend into
underlying subcutaneous tissue.
KELOID &
HYPERTROPHIC SCARS

132. CLINICAL FEATURES
Keloids range in CONSISTENCY from
SOFT and DOUGHY to RUBBERY and
HARD.
Early lesions are often
ERYTHEMATOUS. Lesions become
BROWNISH RED and then PALE as
they age.
Lesions are usually DEVOID of HAIR
FOLLICLES and other functioning
ADNEXAL GLANDS.
KELOID &
HYPERTROPHIC SCARS

133. CLINICAL FEATURES
MOST lesions CONTINUE to GROW
for WEEKS to MONTHS and OTHERS
grow for YEARS.
Growth is usually SLOW, but keloids
occasionally enlarge rapidly, tripling
in size within months. Once they stop
growing, keloids do not usually
cause symptoms and REMAIN
STABLE or INVOLUTE SLIGHTLY.
KELOID &
HYPERTROPHIC SCARS

134. CLINICAL FEATURES
In WHITE persons, keloids tend to be
present, in decreasing order of frequency,
on the FACE (with CHEEK and EARLOBES
PREDOMINATING), UPPER EXTREMITIES,
CHEST, PRESTERNAL AREA, NECK, BACK,
LOWER EXTREMITIES, breasts &
abdomen.
In BLACK persons, the descending order
of frequency tends to be EARLOBES, FACE,
NECK, LOWER EXTREMITIES, breasts,
chest, back, and abdomen.
KELOID &
HYPERTROPHIC SCARS

135. CLINICAL FEATURES
Keloids on the EARS, NECK, and
ABDOMEN tend to be
PEDUNCULATED. Keloids on the
CENTRAL CHEST and extremities are
usually RAISED with a FLAT surface,
and the base is often wider than the
top.
Keloids OVERLYING a JOINT can
CONTRACT and restrict movement.
KELOID &
HYPERTROPHIC SCARS

136. CLINICAL FEATURES
Most keloids are ROUND, OVAL, or
OBLONG with REGULAR MARGINS;
however, some have CLAWLIKE
configurations with irregular
borders.
KELOIDS may be DISTINGUISHED
from HYPERTROPHIC SCARS by
their CLAWLIKE PROJECTIONS,
which are absent in the
hypertrophic scar.
KELOID &
HYPERTROPHIC SCARS

137. CLINICAL FEATURES
MOST patients present with 1 OR
2 keloids; however, a FEW
patients, especially patients with
spontaneous keloids, have
MULTIPLE LESIONS, as do
patients who develop keloids as a
consequence of acne or
chickenpox.
KELOID &
HYPERTROPHIC SCARS

142. Broad, eosinophilic bundles of collagen are the characteristic
finding in keloids, not present in hypertrophic scars

143. Central zone of hyalinized collagen

144. Thick hyalinized collagen bundles

145. HISTOPATHOLOGY
Keloids are comprised of
FIBROBLASTS, FIBROUS TISSUE
which REPLACES NORMAL DERMAL
STRUCTURES, and IRREGULARLY
ARRANGED THICK BANDS of
COLLAGEN in the dermis & SC
tissue.
THICK, HYALINIZED
HYPEREOSINOPHILIC BANDS in the
CENTRAL PORTION of the nodule.
KELOID &
HYPERTROPHIC SCARS

147. PREVENTION
1. Avoid performing nonessential cosmetic
surgery in patients known to form
keloids.
2. Close all surgical wounds with minimal
tension.
3. Incisions should not cross joint spaces.
4. Avoid making midchest incisions, and
ensure that incisions follow skin creases
whenever possible.
5. Use buried sutures, when necessary, for a
layered closure and to reduce tension.
KELOID &
HYPERTROPHIC SCARS

148. TREATMENT
HYPERTROPHIC SCARS generally
SETTLE in TIME OR with
TREATMENT, but KELOIDS may
PERSIST and prove resistant to
treatment.
KELOID &
HYPERTROPHIC SCARS

149. STANDARD TREATMENTS
These include OCCLUSIVE
DRESSINGS, COMPRESSION
THERAPY, and INTRALESIONAL
CORTICOSTEROID INJECTION.
KELOID &
HYPERTROPHIC SCARS

150. TREATMENT MEASURES
1. EMOLLIENTS
2. OCCLUSIVE DRESSINGS
3. COMPRESSION THERAPY
4. SURGICAL EXCISION
5. INTRALESIONAL CORTICOSTEROID INJECTION
6. CRYOTHERAPY
7. SUPERFICIAL X-RAY TREATMENT.
8. LASER THERAPY
9. LIGHT THERAPIES
10. SKIN NEEDLING
KELOID &
HYPERTROPHIC SCARS

151. TREATMENT MEASURES
OCCLUSIVE DRESSINGS, include
silicone gel sheets and dressings,
nonsilicone occlusive sheets,
dressings should be worn for 12
to 24 hours per day.
KELOID &
HYPERTROPHIC SCARS

152. TREATMENT MEASURES
COMPRESSION THERAPY
Mechanoreceptors induce apoptosis
also extracellular matrix. Rigidity
caused by compression may also
inhibit the differentiation and
proliferation of scar fibroblasts
(button compression, pressure earrings,
ACE bandages, elastic adhesive
bandages, compression wraps, spandex
or elastane (Lycra) bandages, and
support bandages)
KELOID &
HYPERTROPHIC SCARS

153. TREATMENT MEASURES
SURGICAL EXCISION (but in
keloids, excision may result in a
new keloid even larger than the
original one) Excisional surgery
alone has been shown to yield a
45-100% recurrence rate.
KELOID &
HYPERTROPHIC SCARS

154. TREATMENT MEASURES
INTRALESIONAL CORTICOSTEROID
INJECTION, as a single modality and as an
adjunct to excision repeated every few
weeks reducing collagen synthesis, altering
glucosaminoglycan synthesis, and reducing
production of inflammatory mediators and
fibroblast proliferation during wound
healing. The most commonly used
corticosteroid is triamcinolone acetonide
(TAC) in concentrations of 10-40 mg/mL
administered intralesionally with a 25- to
27-gauge needle at 4- to 6-week intervals.
KELOID &
HYPERTROPHIC SCARS

155. TREATMENT MEASURES
CRYOTHERAPY - 2, or 3 freeze-
thaw cycles lasting up to 30
seconds repeated every 20-30
days. Insertion of a lumbar
puncture needle through the
long axis of the keloid, from one
side to the other, passing the
liquid nitrogen.
KELOID &
HYPERTROPHIC SCARS

156. TREATMENT MEASURES
LASER THERAPY
Ablative lasers  Carbon dioxide,
argon laser, and Nd:YAG laser
(1064 nm)
Nonablative lasers  Pulsed dye
laser because of its efficacy, safety,
and relatively low cost, the PDL
remains the laser treatment of
choice for hypertrophic scars.
KELOID &
HYPERTROPHIC SCARS

157. MEDICAL TREATMENTS
1. Retinoic acid
2. Intralesional interferon (IFN)
3. Intralesional 5-fluorouracil (5-FU)
4. Intralesional calcium channel blockers verapamil
5. Doxorubicin
6. Bleomycin
7. Imiquimod 5% cream
8. Tacrolimus
9. Tamoxifen
10. Botulinum toxin type A,
11. Over-the-counter treatments (e.g. onion extract;
combination of hydrocortisone, silicon, and vitamin E).
KELOID &
HYPERTROPHIC SCARS

159. LIGHT THERAPIES
1. Photodynamic therapy [PDT]
2. Intense pulsed light (IPL)
3. UVA-1
4. Narrowband UVB
5. Broadband UVB
KELOID &
HYPERTROPHIC SCARS

160. REFERENCES
BOLONGIA DERMATOLOGY ESSENTIALS
BOLONGIA 3rd ed
WEEDON’S SKIN PATHOLOGY
ESSENTIALS
GOOGLE IMAGES
DERMNETNZ.ORG
EMEDICINE.MEDSCAPE.COM

161. THANK YOU
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