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WOUNDCARE WISDOM
WOUND HEALING IN PSORIASIS,
MULTIPLE SCLEROSIS
Wound healing is impaired in both stimulates keratinocyte proliferation,
psoriasis and multiple sclerosis, enhances their expression of VEGF,
raising the prospect that a better and activates their production of
understanding of the process could epidermal growth factor (EGF)
improve our understanding of receptor ligands. The synthesis of
the pathophysiology of these two Stress has EGF results in an autocrine loop and
chronic conditions and generate been reported proliferation of keratinocytes.
targets for treating them. to be a
provoking In psoriasis, the proliferation of
The two conditions share a number factor for keratinocytes does not stop when the
of characteristics. wound has re-epithelialized and in
the first and MS repair of the myelin sheath which
For example, both diseases subsequent protects the nerves is not initiated
demonstrate slight itching, flares of MS or stops before the wound healing
symmetry of the lesions, process is completed.
exacerbation after stopping
corticosteroid treatment, and What goes wrong in psoriasis
the Koebner phenomenon –
provocation of the condition by Elevated intracellular calcium ion
stress. concentrations in keratinocytes
Wound healing occurs in four mean that they do not differentiate,
The Koebner phenomenon stages: significantly increasing the rate of
(isomorphic response) was first wound healing, according to Dr.
described in 1876 by the German • hemostasis Morhenn.
dermatologist Heinrich Koebner • inflammation
who noted that patients developed • proliferation VEGF, a potent stimulator of
psoriasis at sites of excoriations, • maturation angiogenesis, and its receptors
horse bites, and tattoos. VEGFR-1 and -2 have been shown
Keratinocytes and oligodendrocytes to be overexpressed by keratinocytes
Koebner famously saw a psoriatic play key roles in the process. in the suprabasal layers of the
plaque develop on the skin of a epidermis of psoriatic plaques,
farmer where his horse, attempting Keratinocytes are the predominate as well as, by dermal fibroblasts,
to get to the sugar he kept in his cell in the epidermis so must be implying a dermally derived influence
trouser pocket as a treat, had bitten able to respond quickly to repair on neovascularization, she writes.
him, noted Vera B. Morhenn of the any damage. They synthesize a
department of dermatology, San large number of cytokines including Serum VEGF-A concentrations are
Francisco VA Medical Center in San tumor necrosis factor alpha (TNFα), also mACh-R, and can improve
Francisco, California in an article vascular endothelial growth factor wound healing. Benztropine has
for Advances in Wound Care, in a (VEGF), and both the constitutive also been shown to stimulate
review of the relationship between and inducible forms of nitric oxide oligodendrocyte precursor cells’
wound healing, psoriasis and synthase, Dr. Morhenn writes. differentiation and remyelination in an
multiple sclerosis published online animal model of MS.
in Advances in Wound Care.i Oligodendrocytes are non-neural
cells of ectodermal origin that form “The skin-related events appear
“Stress has been reported to be part of the adventitial structure of to mimic the events occurring in
a provoking factor for the first and the central nervous system. the central nervous system when
subsequent flares of MS,” she says. damaged nerves are remyelinated,”
“The occurrence of the Koebner Keratinocytes and oligodendrocytes writes Dr. Morhenn. “That the
phenomenon in psoriasis and produce nitric oxide (NO) – a gas nervous system plays a role in
MS suggests that the etiology of that is important in vasodilation psoriasis is suggested by the finding
both of these diseases may relate and immune andinflammatory that severing of a nerve in one area
to defects in the wound healing responses — and is a vital
process.” component of wound healing. NO 18
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