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Tx Planning and Clinical Practice
Blair Lectures
Desquamative Gingivitis
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Is the term Desquamative Gingivitis a description or diagnosis?
description
area of mouth orthokeratinised:
gingiva
hard
palate
area of mouth parakeratinised?
gingiva
hard
palate
areas of mouth non-keratinised?
lining
mucosa
buccal
mucosa
alveolar
mucosa
soft palate
floor
of mouth
underside
of tongue
when might hyperkeratosis occur?
when
buccal mucosa irritatated
by
smokeless tobacco
or
smoking
how fast do surface layer cells shed?
2.7 hours
what is the differentiation of cells?
how
quickly
they
change
and
mature
what is proliferation of cells?
how
quickly
they
divide
and provide
new cells
what is cellular turnover?
how quickly
cells
divide
and passes through
entire
epithelium
buccal
mucosa
14
days
floor of mouth
20
days
hard
palate
24
days
skin
27
days
desmosomes?
attachments
between
epithelial
cells
rete pegs?
epithelial projections extending
into underlying
connective tissue
hemi-desmosomes?
attachments between
epithelial cells
and
extracellular matrix
of
basal lamina
with autoimmune diseases antibodies work against:
connection between
cells
connections between
tissue layers
what is desquamation?
shedding
of the
outermost layer
of a
tissue
,
natural controlled turnover
process
ulceration
:
discontinuity
or
break
in
bodily membrane
with
loss
of
surface tissue
,
disintegration
and
necrosis
of
epithelial tissue
desquamative gingivitis
initial signs/symptoms of underlying disorder
plaque induced gingival inflammationmay
exacabate condition
and
mask histological features
clinical appearance of desquamative
gingivitis
:
red
glazed gingivae
loss of
stippling
area of
superficial
epithelium desquamation/ulceration
vesicles
,
white
striate,
flecks
may be seen
how do we obtain a diagnosis for desquamous gingivitis?
biopsy
and
histopathology
what might cause desquamative gingivitis?
Lichen Planus
Mucous membrane pemphigoid
Pemphigus Vulgaris
Local hypersensitivity reactions
Plasma cell gingivitis
Orofacial granulomatosis
Epidermolysis Bullosa
(Rare)
Lichen Planus
:
chronic inflammatory mucocutaneous disorder
1.5-2
% of population
middle age
- has been reported in
younger
present on
skin
and
orally
on
mucosa
,
tongue
,
gingiva
,
palate
/
lips
(in
prevelance
order)
Reticular hyperplasia
of
stratum granulosum
Plaque like lichen
planus
Papular
Lichen Planus
Bullous
Lichen Planus
Atrophic lichen
planus
Erosive lichen planus
-
1-5
% potentially
malignant
Histopathology of Lichen Planus:
hyperkeratosis
acanthosis - thickening of
statum
spinosum
liquefaction
degerneation
of
basal
cell
layer (civatte bodies)
dense
subepithelial
band of
T
lymphocytes
elongates,
wide
,
flat
rete
pegs
Epithelium
with
Lichen Planus
Lichenoid Reactions:
dental material
-
antigen fixation
,
lesions
resolve if material
removed
/
replaced
drug erosion
-
history
of
drug taking
,
unilateral
,
atypical
sites,
erosive lesion
?
Histopathology of Lichenoid reactions:
mixed
,
diffused
subepithelial inflammatory infiltrate
perivascular
inflammatory infiltrate
parakeratosis
- nuclei in keratinocytes at surface
civatte
bodies (degenerating)
circulating
basal cell cytoplasmic
antibodies
What drugs can cause lichenoid drug erosions?
antihypertensives
oral hypoglycaemics
non-steriodal anti-inflammatory drugs
seconds line anti-arthritics
xanthines oxidase inhibitors
psychoactive
antiparasitic
antimicrobial
Plasma cell
gingivitis
plasma cell gingivitis:
rapid
onset
sharply
demarcates
affects entire
band
off attached gingiva and may extend to
palate
hypersensitive allergic reaction
- food, flavourings, spices
Histopathology plasma cell gingivitis:
plasma cell undergoing
excessive synthesis
of
Ig
plasma cell
Russel Bodies
- contain Ig
vessel dialation
may mimic:
leukaemia
,
myeloma
,
pemphigoi
plasma cell
gingivitis
Pemphigus:
ages
50
+, fragile
intra-epithelial bullae
(
blisters
),
nikolsky
sign - appear on
pressure
/
friction
histopathology Pemphigus:
IgG autoantibodies
against
PV antigen degrades cell adhesion
identify by
blood test
or
biopsy
Pemphigoid:
ages
50
+, more common in
females
,
sub-epithelial
bullae - at
basement membrane
level, mainly affects
oral
mucosa,
conjunctiva
,
scarring
occurs
How do we identify Pemphigoid?
look at
basement membrane
,
IgG
and
C3 immunofluorescence
Epidermolysis Bullosa
:
collagen protein
defects so cells
rupture
easily,
separate
,
blisters
form
50
in
1 million births
significant
and
debilitating scarring
affects -
oral access
and
dexterity
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