Download - Abdel Hamid Derm Atlas

LICHEN PLANUS: BASAL CELL DAMAGE
The key of understanding lichen planus begins from the basal
cell damage. The disease may be caused by cell mediated
cytotoxic immune reactions that damage the basal cells. A cell
mediated attack of lymphocytes on basal keratinocytes could
cause lichen planus.
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In lichen planus, the number of degenerated keratinocytes may
be so large that they are seen in clusters in the uppermost
dermis. Their aggregation may result in perforation of epidermis
with subsequent trans-epidermal elimination. The damage may
be so large to lead to:
@ Epidermis:
*atrophic
*Perforated.
* Ulcerated
@ Basement membrane zone: vesicle or bulla
@ Skin appendages: Destruction of hair, nail or sebaceous and
sweat glands.
@ Melanocxytes: Damage and presence of melanophages
(post inflammatory hyperpigmentation)
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Because of the importance of this damage, there are a lot of
synonyms to these bodies:
* Colloid
* Hyaline
*Cytoid
*Civatte
*Filamentous
*Sabourod
* Eosinophilic
* Apoptotic.
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All of the following histological changes in lichen planus can be
attributed to the basal cell damage:
@ Hyperkeratosis
@ Focal hypergranulosus
@ Irregular acanthosis
@ Band like dermal infiltrate
@ Focal separation of epidermis from the dermis (Max Joseph
spaces)
Saw toothed contour of rete ridges
@Melanin in dermal melanophages (incontence of pigment)
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There is hypertrophy of epidermal cells but no hyperplasia. A
rough estimate of the number of prickle cells can be obtained by
counting the number of nuclei along the vertical line between
the basal layer and granular layer. Normally 4 -7 nuclei are seen.
This depends on whether one chooses the area above the
papillae or that on rete ridges.
In lichen planus the range is four to seven indicating that there is
no over production (hyperplasia) of cells but there is
hypertrophy. The kertinocytes of prickle cell layer often appear
eosinophilic possibly because of advanced keratinization.
The decreased respiratory enzyme activity, mitochondrial
dysfunction, decreased acid phosphatase and increase lactic
dehydrogenase can be found as a secondary changes to the
disease and not indicative of primary provocative process.
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The basal cell damage in lichen planus is due to an apoptotic
process and not a necrotic one. The following morphological
changes can be seen:
@ The cell shrinks.
@ Loss of normal contact.
@Nuclear changes:
*Nuclear condensation
* Chromatin margination
*Karyorrehexis (nuclear brake down)
@ No mitochondrial or other organelle swelling
@ Lysosomes remain intact
@Apoptotic bodies are formed i.e. enhanced fragmentation
with stable cell membrane).
Necrosis
Stimuli
Apoptosis
By accident
Failure of blood supply
Histology  usually group of cells
Cellular swelling
Karyolysis
Disruption of organelles
Inflammation
DNA
breakdown
mechanism
ATP
depletion
Membrane injury
Free radical damage
By suicide
Physiologic or pathologic
 single cells
 shrinkage
Karyorrhexis
Apoptotic bodies in which
organelles are intact
No inflammation,
phagocytosis of apoptotic
bodies
active process require energy
Internucleosomal
 gene activation
Endonuclease

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Regeneration of basal cell:
A histological observation: in early lesion of L.P. there is
vacuolar degeneration of basal cell. However, in late lesion
the basal layer has the appearance of flattened squamous cell.
This is due to regeneration of degenerated basal cell. There is
migration of epidermal cells from the edge of the lesion &
from adjacent eccrine ducts rather than from increased
mitotic activity to make good cells in the deficit area. The
new basal cells has the appearance of flattened squamous
cells ( spindle shaped or fusiform to spherical).The proof for
that is the little uptake of titrated thymidine at the area of
basal cell damage but conspicuous uptake at the edge of the
lesion.
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The inflammatory infiltrate is band like in nearly 2/3 of cases
of lichen planus and the remaining 1/3 were patchy. The
infiltrate affects the papillary dermis. In active lesion, the
infiltrate obliterates the dermo-epidermal interface and may
actually permeate the lower epidermis itself.
In older lesion, the inflammatory infiltrate is no longer lies in
close approximation to the epidermis.
The dermal infiltrate is largely consist of T cells and very few
of B cells. 4O% of the infiltrate at dermo-epidermal junction
is CD4, where as in dermis they are 8O% of this type of T
cells (CD4). Therefore, CD8 (cytotoxic/suppressor) are
present more in close approximation to dermo-epidermal
junction adjacent to foci of basal cells
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Langerhans' cells are increased in epidermis in early lesion of
lichen planus. This has been taken to indicate that
Langerhans' cells may be processing antigen prior to their
presentation to lymphocytes.
Immune histochemistry of T lymphocytes bound in epidermis
by anti CD2 monoclonal antibody are shown to be in close
contact with epidermal cells and Langerhans' cells .Could this
mean that keratinocytes and Langerhans' cells process an
antigen that leads to T cell activation and ultimately
keratinocyte damage? This suggest cell mediated mechanism
is in operation. Moreover, in the epidermis adjacent to the
infiltrate the basal cells express HLA DR. This enhances the
interaction between lymphocytes and epidermal target cells
resulting in keratinocyte destruction. Probably, these surface
antigen (HLA DR) are induced by cytokine (interferon alpha)
released by the lymphocytes from the infiltrate. The question
is what are the agents which alter the keratinocyte markers of
the host in such a way that they are recognized as foreign and
attacked by T cells?
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Lichen planus is not a single entity. The causative factor (s)
in lichen planus is (are):
@ Vary in its severity:
*From case to case.
* In the same case.
@May be under genetic control.
The causative factor may be aroused by:
* Light (lichen planus actinicus)
* Drugs (lichenoid drug eruption)
*Contact (color developers)
* Mercury in dental amalgam (oral lichen planus)
*Hepatitis C virus in association to lichen planus
particularly in our country with raised infection by this virus.
* We think that anxiety and depression can arouse
lichen planus.
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Q: How can CD8 T cell migrate into epidermis?َ
A: Due to basement membrane disruption. This result from
the effect of mast cell degranulation + matrix metalloprotein
9 which is secreted by T cells.
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