Discussion
Definition of a comprehensive pathophysiological
description of dandruff and seborrheic dermatitis
The signs and symptoms of the D/SD conditions are
well established mainly through traditional (macro) assessment
of the scalp skin condition. The description of
the scalp condition at the structural and molecular level
is now enabled by new molecular measurement capabilities.
The pathophysiological model that is emerging
(Fig. 1) is based on the established etiological phases
of Malassezia metabolism initiating the inflammatory
cascade, resulting in scalp skin hyper-proliferation and
incomplete corneocyte differentiation that yields an
impaired SC barrier.
Measures at the structure/function level, such as
epidermal morphology, Malassezia infiltration and
instrumental assessments related to moisture content
have supported the basic etiology sequence discussed
above. These measures have enabled a deeper understanding
of the pathophysiology of these conditions by
demonstrating that the superficial signs and symptoms
are the result of an irregular epidermal construction
and resultant dis-organization in the onset of D/SD.
These observations, in turn, have led to probing specific
molecular mechanisms in the skin, which established
the inflammatory nature of the condition, the poor synchronization
of proliferation and differentiation and the
relatively ineffective barrier function.
Rather than describing a healthy scalp as simply being
free from signs and symptoms of a condition, these new
parameters enable both a more complete pathophysiological
description of D/SD as well as establishing more
specific criteria for assessing whether the condition has
been effectively treated.
DiscussionDefinition of a comprehensive pathophysiologicaldescription of dandruff and seborrheic dermatitisThe signs and symptoms of the D/SD conditions arewell established mainly through traditional (macro) assessmentof the scalp skin condition. The description ofthe scalp condition at the structural and molecular levelis now enabled by new molecular measurement capabilities.The pathophysiological model that is emerging(Fig. 1) is based on the established etiological phasesof Malassezia metabolism initiating the inflammatorycascade, resulting in scalp skin hyper-proliferation andincomplete corneocyte differentiation that yields animpaired SC barrier.Measures at the structure/function level, such asepidermal morphology, Malassezia infiltration andinstrumental assessments related to moisture contenthave supported the basic etiology sequence discussedabove. These measures have enabled a deeper understandingof the pathophysiology of these conditions bydemonstrating that the superficial signs and symptomsare the result of an irregular epidermal constructionand resultant dis-organization in the onset of D/SD.These observations, in turn, have led to probing specificmolecular mechanisms in the skin, which establishedthe inflammatory nature of the condition, the poor synchronizationof proliferation and differentiation and therelatively ineffective barrier function.Rather than describing a healthy scalp as simply beingfree from signs and symptoms of a condition, these new
parameters enable both a more complete pathophysiological
description of D/SD as well as establishing more
specific criteria for assessing whether the condition has
been effectively treated.
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