Good Morning

By Ibrahim Gbr
 1.Case Report.
•The 55-year-old female patient attended the outpatient clinic
of the oral and craniomaxillofacial surgery department for
treatment of multiple painful nodules of her lip mucosa. On
admission, the patient was in excellent general health and had
no history of further diseases. She reported to have noticed an
unspecific pressure on her lips during the preceding years but
could not detail the history of her symptoms or the palpability
of her findings. She denied any history of viral affection of the
oral region. External examination showed no alteration of the
lips. Oral examination revealed multiple nodules, painful on
palpation, below the non-inflammatory mucosa of the upper
and lower lip. Enlarged ostia were visible that secreted a clear
tenacious mucus.
Cheilitis glandularis.
 chronic
inflammatory condition of the minor salivary glands,
predominantly of the lower lip.
Clinical Signs
• Swelling of lower lip due to Hyperplasia and infiltration
of the gland
• Eversion of lower lip leading to crusting of mucosal part
• The orifices of minor salivary glands are Dilated
• Pressure on lip may produce mucouse or mucopustular
Fluids from ductal opening.
Histopatholog
y
• Atrophic labial gland with
dilated ducts were scattered
among Fibrosis
• Inflammatory changes of minor
salivary gland associated with
lymphatic infiltration
• can be considered a potential
predisposing factor for the
development of actinic cheilitis
and squamous cell carcinoma.
Case Report 2
 2.Case Report
A 43-year-old woman patient presented with
persistent, painful upper lip swelling since one week.
There was no history of applied irritants, local trauma
or atopy. She also reported burning and peeling off in
perioral area. Past history revealed that patient had
been treated for similar condition with various
different modalities including ayurvedic medication,
homeopathy and topical steroids in past three years.
On examination the upper lip and perioral area
showed painful swelling, with areas of crusting and
fissuring Neither facial nerve palsy nor fissuring of
the tongue nor lymph node involvement was present.
No such lesions were seen intraorally.
 Condition Related to
Granulomatous cheilitis???
Melkersson-Rosenthal syndrome.
Granulomatous Cheilitis
Clinical Signs.
• chronic swelling of the lip due to
granulomatous inflammation.
• Non tender swelling
• Fissured with reddish brown discoloration with
scaling
• Related to Melkersson Rosenthal syndrome
associated with
1. fissuring of the tongue
2.  facial paralysis 
Granulomatous Cheilitis

Histopathology
• chronic inflammatory cells infiltrate
•  Mild acanthosis of the epidermis and scattered
(acanthosis mean increase number of specialized
squamous cells in skin)
• Peri and para vascular aggregations of Lymphocytes
Plasma cells and Histocytes
• Formation of epitheloid cells and Langhans type giant
cells leading to Granulomatous infiltration
Case Report 3
 3.Case Report
•A 32-year-old male patient visited your
clinic complaining of multiple small
granules on his buccal mucosa. The
granules were flesh-colored and partly
confluent . These granules are typically
no more than 1-2mm in diameter.
 Fordyce’s granule
Clinical Signs
• Ectopic lesion (sebaceous gland present in oral
tissue)
• Yellow-white, asymptomatic
•  1 - 3 mm papules that remain constant
throughout life
•May be hyperplastic and nodular
• Most common seen in buccal mucosa and lateral
portion of the vermilion of the upper lip
 Fordyce’s granules

•Histopathology
• Similar to normal sebaceous gland in
skin except there is no hair follicles
• Acinar lobules can be seen beneath the
epithelial surface
• Connected to surface through a central
duct
•Parakeratotic stratified squamous
epithelium overlies the sebaceous lobules
Case Report 4
4.Case Report

The patient was a 21-year-old male with “white, itchy spot”

on the buccal mucosa. White bilateral lesion in oral mucosa
was the chief compliant of the patient. The patient
complained of a white lesion which was present since birth.
The patient’s general health was reportedly good.
In clinical examination, there were bilateral, symmetrical
white plaques and patches on the buccal and labial mucosa,
which could not be removed . The plaques were smooth with
velvety texture and irregular, well-defined borders. There
was no elevation or erythema. The margins were clear and
no lymph nodes were noticeable. Oral hygiene was good and
other oral structures were normal in appearance.
White sponge Nevus
Clinical Signs
• Hereditary (autosomal dominant disorder)
•  usually appear at birth or in early childhood,
but sometimes the condition develops during
adolescence. 
• The lesions consist of symmetric, thickened,
white, corrugated or velvety, diffuse plaques.
• Patients are usually asymptomatic.
• Usually  bilateral, symmetrical white plaques
White sponge Nevus
Histopathology
• Acanthosis and hyperparakeratosis
• hyperplasia of prickle cell layer )
• There is intracellular oedema and
intercellular oedema which give basket
weave appearance
• Intact basal cell layer
• Mild inflammatory cell infiltrates Upper
dermis
Difference between:
Case Report.5
 5.Case Report

A 65-year-old male patient presented to

your clinic due to notion of alternation
in tongue pigmentation ͕ with about 1
month of evolution and associated
complaints of oral discomfort and
xerostomia.
 Hairy Tongue.

•Clinical Sign
• enlargement and discoloration of the filiform papillae
which are hypertrophied
• Absence of an adequate peeling of the keratin layer on
filiform papillae leading to Hyperkeratosis
• Filiform papillae can reach between 12-18 mm
• Hairy tongue is usually asymptomatic
• Brown, black, green or yellow discoloration may be
present.
 Hairy Tongue

Histopathology.
• Markedly elongated filiformm papillae with
hair-like spires of keratin
• Hyperkeratosis
•Basophilic bacterial colonies often adhered to
keratin surface.
Predisposing Factor
• poor oral hygiene
• medications (especially broad-spectrum
antibiotics)
• radiation therapy of the head and neck 
• Tobacco smoking
•  coffee and heavy black tea consumption
Case Report.6
 6.Case Report
A 50 year old female from the presented in the clinic with one
month history of mild pain and burning sensation on the tongue
which aggravated on intake of citrus and spicy foods. She also
complained of discomfort during chewing and malodor. Medical
and family history were non-contributor. Extra-oral
examination revealed normal facial morphology, no skin lesions
were seen. Intra-oral examination revealed poor oral hygiene,
halitosis and deeply grooved lesions on the dorsal surface of the
tongue with entrapped food debris. Flushing was done on the
tongue surface with diluted povodine-iodine solution which
revealed numerous prominent fissures covering the entire dorsal
surface and dividing the tongue papillae into multiple separate
lobules. No other tongue lesion or associated syndrome was
observed.
fissured tongue
Clinical sign
• The etiology is unknown but hereditary plays a
significant role. 
• may become apparent during childhood or
later in life
• It may be related to syndromes or Familial
conditions like
1.  Melkersson-Rosenthal syndrome
2.  Down syndrome
3. Acromegaly
4. Sjorgen’s syndrome
•  fissured tongue can be classified as median and
lateral types
Fissured Tongue.

Histopathology
• increase in the thickness of lamina
propria
• hyperplasia of rete-pegs.
• neutrophillic micro-abscess in the
upper epithelial layers
•  inflammatory cells infiltrate in
lamina propria
 Difference Between

Fissured Tongue Geographic Tongue

•  benign condition characterized by inflammation
• The etiology is unknown but of the tongue.
hereditary plays a significant role. • appears in a map-like (geographic) pattern.
• the condition is usually painless. Some •  certain areas of the tongue are missing papillae
individuals may complain of an so it appear smooth , red or pink colored
associated burning sensation.  (erythematous)
•   There are usually multiple grooves • .Most cases are not associated with any
symptoms (asymptomatic).
• harmless condition usually with no • the condition usually goes away without
associated symptoms. No treatment is treatment.
necessary except to encourage good oral • Associated with psoriasis
hygiene
Case Report.7
7.Case Report

A 78-year-old male patient reported to the outpatient

department, with a complaint of white patch on the right
lateral border of the tongue for one month. Oral
examination revealed a homogenous greyish white
plaque on the right ventrolateral border . The surface
showed cracked mud appearance and on palpation the
lesion felt as raised and rough. The lesion was non tender
and non scrapable. Lips, buccal mucosa, pharynx, and
extra oral soft tissues appeared normal. The patient was
neither under any medication nor had any tobacco
associated habits. Dental examination revealed crowns
No sharp margins were evident on palpation of these
crowns.
Leukoplakia
Clinical sign
• The symptoms of leukoplakia are one or more white patches on
the surface of the tongue, underneath the tongue, or on the
insides of the cheeks.
• Asymptomatic
• Premalignant and can turn to squamous cell carcinoma.
• Factors that are strong indicators of leukoplakia transforming to
cancer include the appearance of:
1.Nodules.
2.White or red masses with a pebbled appearance.
3.Ulceration.
4.Increased firmness.
5.Bleeding.
What are the types of leukoplakia?

1. Homogenous: A mostly white, evenly colored thin patch that may have
a smooth, wrinkled, or ridged surface that is consistent throughout.
2. Non-homogenous: A mainly white or white-and-red, irregularly shaped
patch that may be flat, nodular (having protrusions), or verrucous
(elevated). 
3. Proliferative verrucous leukoplakia (PVL): is a rare but especially
aggressive form of oral leukoplakia. usually diagnosed late in the
development of leukoplakia, as it takes time to spread to multiple sites.
It also has a high rate of recurrence.
4.  oral hairy leukoplakia : This condition looks like its name—white hairy
patches, often with folds so it looks like hair is growing out of the
folds. Oral hairy leukoplakia doesn’t become cancer.
NB : Non-homogenous leukoplakia is seven times more likely to become
cancerous than the homogenous type.
Leukoplakia
Histopathology
•Compact hyperkeratosis with hypergranulosis
•Epithelial atrophy or hyperplasia
•approximately 33% of dysplasias are
characterized by an inflammatory infiltrate
and should not be misdiagnosed as 
lichen planus
•Leukoplakia with dysplasia exhibits
characteristic architectural and cytological
features of keratinizing dysplasia