12/4/2016

Classification
• Aesthetic pits
conditions • Blisters
• Cleft lip and palate •
Lip disorders (CLP)
Herpes labialis
• Erythema
• Body art Multiforme
• Cicatrization
• Lip fissure
• Lip dimples and

• Inflammatory • Contact • Ulcerative granulomatosis

(Cheilitis) • Nutritional • Basal cell • Ascher syndrome
• Actinic carcinoma • Angiodema
• Simplex
• Angular • Squamous cell • Keratoacanthoma
• Traumatic carcinoma
• Exofoliative • Silicone granuloma
• Swelling
• Glandular • Mucocele
• Plasma cell • Orofacial

• White lesions
• Fordyce's spots
• Vitiligo Aesthetic conditions
• Morsicatio labiorum/buccarum
• Pigmented lesion
• Melanotic macule
• Venous lake

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Body art
• Etiology Tattooing or piercing with an
objects are common in certain Cultures
• Clinical features
• Skin, vermilion and inside the lip.
• Maxillofacial Tattooing Examples: Chin
Tattooing in Maoris, vermilion red
tattooing in Western countries, skin
tattooing at the angle of the mouth in
wodaabe people, lower lip tattooing in
Sudanese women.
Cicatrization
• Scarring and sometimes deformity may
follow tissue destruction by, for
example:
• burns, lacerations and gunshot wounds
• Irradiation and after lip surgery
• Skin diseases (e.g. epidermolysis bullosa
and toxic epidermal necrolysis) or
infections such as cancrum oris.
• Self mutilation
• Other features of this syndrome may
include hypodontia, congenital heart
disease, cerebral abnormalities,
syndactyly and ankyloglossia
• Surgical removal may sometimes be
indicated for pits
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• Maxillofacial piercing usually associate
with other forms of body art
• Jewellery, usually stainless-steel studs,
rings or barbells is placed in the lower lip,
tongue or other areas in the head and
neck.
• Complications of maxillofacial piercing
include mainly pain, bleeding, infection,
dental fractures and gingival damage.
Systemic infections are rare.
Lip dimples and pits
• Dimples, a facial muscle deformity of
zygomaticus major, are common at
cheeks or chin.
• Congenital lip pits are rare, typically
seen in females, on the lower lip, and
often associated with clefting disorders
(Van der Woude syndrome).
Lip fissure
• Etiopathogenesis children mouth
breather, sun, wind, cold weather,
smoking, hereditary, down syndrome,
OFG
• Clinical features Males
• Median lower lip fissures are chronic,
causing discomfort and sometimes,
bleeding.
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• Diagnosis Clinical
• Management correct predisposing
factors if possible.
• Bland creams
• If fails to heal, excision.
Erythema Multiforme
• Etiology Hypersensitivity reaction to
infectious agents, drugs, or idiopathic
• Minor form (less severe) usually triggered
by herpes simplex virus
• Major form (Stevens-Johnson syndrome)
often triggered by drugs (e.g. NSAID,
antibiotics and anticonvulsants)
• Other factors malignancy, autoimmune
disease, food additives, vaccination and
radiotherapy)
• Most patients have oral lesions which begin
as erythematous macules that blister and
break down to irregular, extensive, painful
erosions and ulcerations with surrounding
erythema, typically in the anterior mouth
• The labial mucosa is often involved, and a
serosanguinous exudate leads to crusting
or blood staining of the swollen lips
(pathognomonic).
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Blisters
• Clinical Presentation young adults males
• Spring or fall
• Acute onset of multiple, painful, shallow
ulcers and erosions with irregular margins
• Symptoms range from mild discomfort to
severe pain
• Self limiting but recurs in about 25%
• Attacks usually lasting 10–20 days,
occurring once or twice a year and resolve
after about 6 episodes.
Types of EM
• EM minor accounts for 80% of cases,
presents as mild, self-limiting rash
affecting only one site (mouth or skin or
other mucosae)
• EM major (Stevens–Johnson syndrome)
severe, life-threatening variant that
overlaps with toxic epidermal necrolysis
(see below) and involves multiple mucous
membranes and epithelia.
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• Features include:
• Fever
• Ocular changes (conjunctivitis, uveitis, dry
eyes and symblepharon). In advanced
cases, lacrimation, photophobia, scarring
and blindness may ensue
• Genital lesions (balanitis and urethritis).
Painful vulval ulcers may result in urinary
retention
• Diagnosis mainly clinical, Nikolsky sign is
negative. There are no specific diagnostic
tests.
• Biopsy can help, but not always diagnostic
• Differential Diagnosis Viral infection, in
particular, acute herpetic gingivostomatitis
(Note: Erythema multiforme rarely
affects the gingiva), Pemphigus vulgaris,
Major aphthous ulcers, Erosive lichen
planus, Mucous membrane pemphigoid
• Minor EM symptomatic treatment and
topical corticosteroids. However,
systemic corticosteroids may still be
required.
• Major EM systemic corticosteroids
and/or azathioprine or other
immunomodulatory drugs.
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• Bronchopulmonary and renal involvement
may also be seen.
• Rashes of various types (hence termed
‘EM’).
• The characteristic rash consists of
‘target’ or ‘iris’ lesions in which the
central lesion has a surrounding ring of
erythema.
• In EM major, Rash may be bullous.
• Management Spontaneous healing can be
slow—up to 2–3 weeks in minor EM and
up to 6 weeks in EM major.
• Precipitating factors, when identified,
should be treated (Chlorhexidine
mouthwash, Aciclovir in Herpes simplex
virus associated erythema multiforme
(HAEM)
• Toxic epidermal necrolysis (TEN) a rare,
potentially lethal mucocutaneous condition
in which the skin peels off in swaths, with
30% or more epithelial detachment.
• Stevens-Johnson syndrome (SJS) a milder
form, with epithelial detachment involving
less than 10% of body surface.
• Both TEN and SJS usually affect the
mouth, and early on.
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• They involve two or more mucosal
surfaces and present with blisters that
arise on erythematous or purpuric
macules. Fever is common.
• Mucous membrane involvement can
result in gastrointestinal hemorrhage,
respiratory failure, and ocular and
genitourinary complications.
• Treatment is withdrawal of culprit
drugs, and urgent specialist referral to
a burns or intensive care unit for
treatment (with intravenous
immunoglobulins, ciclosporin,
cyclophosphamide, plasmapheresis,
infliximab)
• Supportive management and nutritional
support.
Herpes Labialis (cold sores)
• Etiopathogenesis Reactivated of Herpes
simplex virus by factors such as: fever,
sunlight, trauma or immunosuppression.
• Clinical features Lesions at
mucocutaneous junction, starting as
macules then papules, then vesicles,
then pustules over a few days with
crusting and healing without scar.
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• Typically these conditions arise as
adverse drug reactions (e.g. NSAIDs,
antiretrovirals carbamazepine and
sulfonamides).
• These conditions must be
differentiated mainly from
paraneoplastic syndromes.
• Diagnosis is largely clinical, though viral
studies can be done
• Differential diagnosis primary HSV
infection, zoster, impetigo or carcinoma
(rarely).
• Management spontaneous remission within
1 week to 10 days
• Penciclovir 1% cream in the prodrome.
• Systemic antivirals (aciclovir) for severe
or immunocompromised cases
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Cheilitis
• Diagnosis history, Clinical and Biopsy
• Differential Diagnosis Exfoliative cheilitis,
Squamous cell carcinoma
• Treatment Prevention of further damage
(broad-brimmed hats, and using adequate
UV-protective sunscreens and avoiding
mid-day sun exposure)
• Topical 5-fluorouracil or vermilionectomy
for severe disease
• Regular monitoring
Contact Cheilitis
• Etiopathogenesis lipsticks, lip salves,
tartar-control toothpastes,
mouthwashes, dental materials, foods
and flavourings, cane reed instruments.
• Clinical features There may be labial
erythema, edema, vesicles, crusts,
scales or fissures
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Actinic cheilitis (actinic keratosis of
lip, solar keratosis, solar cheilosis)
• Etiology Chronic, excessive sunlight
• exposure
• Clinical Presentation Vermilion portion of
lower lip
• Older white males
• Pale irregular keratotic surface with
intervening red (atrophic) zones
• More advanced lesions are scaly, crusted
and/or indurated.
• Progression to carcinoma in 6% of cases
Chapping of the lips (cheilitis
simplex or common cheilitis)
• Etiopathogenesis exposure to freezing cold or
hot, dry winds.
• Clinical features The lips become sore, cracked
and scaly and the affected subject tends to
lick the lips, or to pick or chew at the scales,
which may aggravate the condition
• When chronic, crusting and bleeding develop
• Diagnosis Clinical.
• Management avoid causative environmental
conditions.
• emollients
• Diagnosis Clinical, if allergic reaction is
suspected, skin patch tests
• Management identify and avoid
offending substance
• Short course of topical fludrocortisone
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Exfoliative Cheilitis
• Etiology factitious (stress), infections
(candidiasis and HIV), atopic eczema
• Clinical Presentation Girls or young
women
• Starts in the center of the lower lip and
spreads to involve the whole of the
lower or of both lips.
• Diagnosis history and Clinical, biopsy is
sometimes indicated
• Differential Diagnosis Actinic cheilitis,
Contact cheilitis, lupus erythematosus
• Treatment Determination of cause and
reassurance
Glandular cheilitis
• Etiology Idiopathic inflammation of minor
salivary glands with mucus hypersecretion.
• In a few cases, familial or due to irritation
(e.g. actinic damage, repeated licking)
• Clinical features Lower lip mainly
• Lips are swollen, enlarged with pinhead
orifices from which mucus saliva can be
squeezed.
• In some cases, erosion, crusting, pain and
abscess can be noticed
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• Patient may complain of irritation or
burning and can be observed frequently
biting or sucking the lips
• Lip is covered with a shaggy yellowish
coating.
• Scaling and crusting (mainly in vermilion
border) persisting in varying severity
for months or years.
• Some cases resolve spontaneously or
with improved oral hygiene but often
exfoliative cheilitis is refractory to
treatment
• Topical corticosteroids.
• Psychiatric consultation if factitial
cause is suspected (some cases regress
with antianxiolytic or antidepressant
treatment)
• SCC arises in 20–30% of cases.
• Diagnosis Biopsy.
• Management Systemic corticosteroids
• Lip balms and sunscreens.
• In advanced disease, surgery, because
of the risk of malignancy.
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Plasma cell cheilitis (plasma cell
orificial mucositis)
• Etiopathogenesis rare inflammatory disorder of
the lips with plasma cells infiltrate in the upper
lamina propria/dermis.
• Similar conditions (under a variety of names)
can affect the penis, vulva, buccal mucosa,
palate, gingiva, tongue, epiglottis and larynx.
• The cause is unknown, presumably
immunological. Precipitants may include a range
of substances such as additives to cosmetics or
dentifrices.
• Diagnosis Biopsy (plasma cell dyscrasia
should be excluded)
• Patch testing to exclude contact
hypersensitivity factors.
• Management treat the underlying cause if
possible
• Topical clobetasol or intralesional
triamcinolone
• Systemic corticosteroids can also help.
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• Clinical features lower lip of an elderly
person
• Glistening red circumscribed flat or
raised patches.
• Fissuring, ulceration and pain
• Plasmoacanthoma, an advanced version
of Plasma Cell Cheilitis (in a form of
verrucous tumor), candida albicans may
be found along the angles of the mouth
Nutritional and traumatic
cheilitis
• Nutritional pellagra deficiency
• Shiny cracked or eroded vermilion
• Milder degrees of deficiency cause
angular cheilitis, oral ulcers and glossitis
• Traumatic e.g. habits such as lip-licking
and use of various musical instruments
Swellings
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Orofacial Granulomatosis
Granuloma inability of macrophages to destroy certain pathogens or foreign
bodies (central zone of macrophages, epithelioid cells and giant cells
surrounded by lymphocytes and fibrous tissue).

• a condition characterized by persistent

non tender enlargement of orofacial
soft tissues.
• Etiology Unknown, theories include
genetic predisposition, allergy and
infection
• Genetics Debate about link with HLA
antigen

• Allergy to: dental material (cobalt and
mercury in amalgam).
• Food additives and preservatives in food
(e.g. benzoates) some foods such as
margarine, eggs, chocolate or menthol.
• Infection e.g. Mycobacterium
tuberculosis, Mycobacterium
paratuberculosis.
• C/Fs children and young adult, more
common in males.
• Classic presentation is a nontender,
recurrent labial swelling that eventually
becomes persistent.
• When severe, may lead to median
cheilitis and/or angular cheilitis.

• Enlargement involves (one or both lips)
and one or both cheeks (initially soft
then becomes firmer with time till
fibrosis ensues).
• Involvement of the lips alone is called
cheilitis granulomatosa (of Miescher).
• Forehead, eyelids or one side of the
scalp may be involved as well or in
isolation.
• Chronic Painful linear ulcers in sulcus or
vestibules with wide erythematous
margins and granulomatous masses
flanking them. Less common type is
superficial aphthous like ulcer on any
mucosal surface.

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• mucosal ‘cobblestones’ (in the cheek and
sometimes in the palate)
• mucosal tags (deep in fold between gum
and inside cheek or lips, vestibules or
retromolar region)
• Perioral skin may become dry, red and
peeling.
Melkersson–Rosenthal syndrome
• Rare neurological disorder
• 300 cases reported (M>F).
• Unknown etiology, genetic predisposition?
(high prevalence among Bolivians).
• childhood or early adolescence.
• Recurring facial palsies (in 30%), swelling
of the face and lips (usually the upper lip),
and fissured tongue (in 20-40% but may
present since birth).
• Differential Diagnosis acquired and
hereditary angioedema, Melkersson–
Rosenthal syndrome, Crohn disease,
sarcoidosis, Lymphomas, granulomatosis
with polyangitis (rarely), Infections
(tuberculosis, leprosy, leishmaniasis),
Foreign body reactions, dental abscess
and trauma.
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• Gingival enlargements with erythema,
can be localized or generalized, varies in
color from normal to salmon pink to red.
• Other features that may present
include fever, headache, visual
disturbance, loss of taste, decreased
salivary gland secretion and cervical
lymphadenopathy
• Facial palsy is of lower motor-neuron type.
It can be unilateral or bilateral, partial or
complete.
• Occasionally, other cranial nerves palsies
may be invloved (e.g. olfactory, auditory,
glossopharyngeal, hypoglossal).
• Symptoms recur intermittently after first
attack. Sometimes develop a chronic
course.
• Follow-up to exclude Crohn's disease or
sarcoidosis.
• Investigations Patch tests to exclude
reactions to various foodstuffs or
additives (Elimination diets can be
diagnostic)
• Blood tests, endoscopy, radiography
biopsy to exclude crohn’s disease
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• Chest radiography, serum angiotensin
converting enzyme, gallium scan,
increased calcium level, tuberculin skin
test, labial salivary gland (shows
granuloma in 20%) to exclude
Sarcoidosis
• Lip Biopsy
• Chlorohexidine mouth wash to prevent
infection and moisturizers for dry skin.
• Other options inlcude clofazimine,
NSAIDs, metronidazole,
hydroxychloroquine, mast cell
stabilizers, or low-dose methotrexate.
• Rarely, cheiloplasty is indicated.
• Heerfordt syndrome (salivary and lacrimal
swelling, facial palsy and uveitis) is rare.
• Occasional association with Sjögren
syndrome.
• Diagnosis lesional biopsy, chest imaging,
gallium scan, raised serum angiotensin
converting enzyme.
• Management Intralesional or systemic
corticosteroids, corticosteroid-sparing
immunosuppressives.
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• Treatment Spontaneous remission can
occur but is rare.
• Elimination diets (50% will respond),
specialist referral if crohn or sarcoidosis
are suspected
• Simple compression or compression devices
may reduce lip edema
• Topical steroid or intralesional
triamcinolone
• Short course of systemic corticosteroids
for severe cases
SARCOIDOSIS
• A rare multisystem chronic
granulomatous reaction of unknown
aetiology
• Clinical features young black females.
• Cervical lymphadenopathy, oral mucosal
nodules, gingival hyperplasia, or labial or
salivary gland swellings/masses, or
xerostomia
• Involvement of lung, liver, skin, bone
Crohn’s disease
• Chronic inflammatory bowel disease
• affects mainly ileum, but can affect any
part of GIT including the mouth.
• Etiopathogenesis unknown.
• Suggestions include mycobacterium
paratuberculosis infection.
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• C/Fs childhood and young adults, M > F.
• Facial and /or labial swelling.
• Extraoral features include abdominal
pain, persistent diarrhea with passage
of blood and mucus, anemia, and weight
loss (all absent in OFG).
• Oral lesions (same as those in idiopathic
OFG) are most likely in those who
develop skin, eye or joint complications.
• Management treated by a physician
(secondary deficiencies correction, diet
elimination, intralesional or systemic
steroids)
• In some circumstances, resection of areas
of intestinal lesions is indicated.
• Some patients with OFG may develop
Crohn’s disease months or years later.
• Regular follow-up should ensure that
systemic disease is recognized early.
Angioedema
• Rapid development of edema of the lip(s),
tongue and oral or facial swelling
• Potentially lethal
• Usually allergic (type 1 hypersensitivity in
those with atopy) but can rarely be drug-
induced, hereditary (hereditary angio-
neurotic oedema or HANE; caused by a
deficiency of the complement C1 esterase
inhibitor – C1-INH) or C1-INH deficiency
can be acquired.
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• Investigations blood tests (FBC,
albumin, calcium, folate, iron and vitamin
B12 may reveal malabsorption)
• Imaging (barium enema, sigmoidoscopy
and colonoscopy)
• biopsy Negative result cannot
necessarily exclude the condition.
Ascher syndrome
• Repeated episodes of lip and eyelid
edema and occasionally goiter (non
toxic, usually presents several years
after initial eyelid and lip edema).
• Childhood and young adults.
• Lip swelling is caused by redundant
salivary tissue and is associated with
blepharochalasia
• Treated with cosmetic surgery
• Allergic angioedema
• Etiopathogenesis type 1 hypersensitivity
reaction, induced by: Foods (nuts mainly
but shellfish, eggs, milk may be implicated)
• Latex, contrast medium, hepatitis B
immunization, insect bites/stings.
• Drug induced form in caused by angiotensin
converting enzyme (ACE) inhibitors
antidepressants, NSAID and antibiotics
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• C/Fs Adult females
• Acute edema < 2 h of antigen exposure
• Itchy labial and periorbital swelling
(may be associated with anaphylactic
reactions) that can involve any oral site.
• When involves tongue, neck and extends
to larynx, can cause respiratory
obstruction.
• If mild angioedema, oral antihistamines
or ephedrine
• Rare intractable chronic cases may
respond to systemic corticosteroids.
• Severe cases may need intramuscular
adrenaline with systemic
corticosteroids and/or antihistamines.
• C/Fs any age, less common but more severe
• Blunt injury or dental trauma are potent
triggers.
• Abdominal pain, nausea or vomiting,
diarrhoea, rashes and peripheral oedema
sometimes herald attacks
• Acute onset of non-itchy or painful oedema
of lips, tongue, mouth, face and neck
region, extremities and GIT.
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• Diagnosis Clinical, history of atopic
disease and/or exposure to allergen
• Blood tests, Low C4 level but normal C1
and C3.
• Management ensure a patent airway
(endotracheal intubation or
tracheostomy if needed).
• Causal substance should be discontinued
• HANE (C1 esterase inhibitor
deficiency)
• Autosomal dominant, SERPING1 gene
mutation
• Attacks are precipitated by alcohol,
cinnamon (which are vasodilators),
stress and NSAIDs
• May persist for up to 4 days,
involvement of the airway is a risk
(Mortality is 30% if left untreated)
• Diagnosis family history
• Clinical features with a history of
oedema after trauma
• Blood tests: low C4, normal C3, absent
of C1.
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• Treatment avoid triggers
• C1-INH replacement.
• Fresh plasma, tranexamic acid, or
androgenic steroids
Keratoacanthoma
• Etiology squamoproliferative lesion of
unknown cause.
• Suggestions include sun damage, viruses
(HPV), chemical carcinogens, trauma,
and Immunosuppression
• Clinical Presentation Mainly in skin (sun-
exposed sites), rare intraorally
• Asymptomatic, solitary or multiple
• Diagnosis Clinical and biopsy (may
resemble squamous cell carcinoma in
histology)
• No reliable clinical, or histologic criteria
to differentiate these two lesions.
• Differential Diagnosis Squamous cell
carcinoma, Molluscum contagiosum,
Verruca vulgaris, solar keratosis,
Condyloma acuminatum.
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Silicone granulomas
• Caused by dimethylpolysiloxane filler or
other fillers for soft tissue
augmentation, inducing a granulomatous
inflammatory response.
• Diagnosis can be challenging (resembles
liposarcoma)
• Treated with topical imiquimod
• Small red macule then firm papule then
nodule with central keratin core (growth
over approximately 4 to 8 weeks)
• Occasionally regresses spontaneously with
a superficial scar.
• Multiple keratoacanthomas are a feature
of the Muir-Torre syndrome, an autosomal-
dominant skin condition of genetic origin
characterized by cutaneous tumors of the
sebaceous gland and visceral malignancy
• Treatment because of difficulties in
diagnosis and distinction from squamous
cell carcinoma, careful observation and
regular follow-up is needed.
• Surgical excision or thorough curettage
(recurrence is rare).
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Ulcerations
• Slow growth, locally destructive and
rarely metastasizes
• Forms include noduloulcerative,
pigmented, superficial and fibrosing
• Diagnosis Biopsy
• Treatment Mostly surgical
• Clinical features Older white males
• Lower lip
• Thickening, induration, crusting or
ulceration, usually at the vermilion border
just to one side of midline. However, other
presentations can be seen (e.g. nodule,
ulcer, red plaque, white plaque, fissure)
• Metastasis is primarily to submental and
submandibular lymph nodes.
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Basal Cell Carcinoma
• Commonest skin cancer as well as of the
head and neck.
• Predisposed by chronic sun exposure
and hereditary syndromes (e.g.
odontogenic keratocysts)
• C/Fs Older white males
• Non–hair-bearing skin.
Lip cancer
• Etiopathogenesis chronic sun exposure,
actinic cheilitis
• Other factors may include low socio-
economic class, tobacco smoking,
syphilis, poor dentition, infection with
HSV and HPV and immune suppression
• Genetic risk factors include xeroderma
pigmentosum, epidermolysis bullosa,
albinism, DLE and cheilitis glandularis.
• Diagnosis Biopsy
• Differential diagnosis herpes labialis,
keratoacanthoma, basal cell carcinoma and
chronic infections such as deep mycoses.
• Determine whether cervical lymph nodes
are involved, or if there are other primary
neoplasms in the upper aerodigestive tract,
or metastases elsewhere.
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• Management Surgery and/or irradiation.

• Patients tend to present with a good
prognosis (5-year survival rates range
from 70% to 90%)
Pigmented lesions

Venous lake (varix, senile

hemangioma)
• Etiopathogenesis Venous dilatation.
• Clinical features solitary bluish-purple
soft fluctuant swelling, 2–10 mm in
diameter, usually seen on the lower lip White lesions
vermilion of an elderly person.
• Diagnosis Clinical
• Management Monitoring for most cases
or excision

Morsicatio buccarum/Labiorum (cheek and

Fordyce’s Granules
• Etiology Ectopic sebaceous glands
• Clinical Presentation Asymptomatic
multiple, scattered, yellowish pink,
maculopapular granules
• Buccal mucosa and lip vermilion
• Diagnosis Clinical
• Treatment Reassurance
lip chewing)
• Etiology seen in anxious patients and
psychologically related disorders (e.g. TMD)
• Clinical features Shaggy, white, keratotic
surface on a reddish background.
• lower labial mucosa and/or buccal mucosa
• Diagnosis clinical plus biopsy
• Differentiate from Leukoedema, Leukoplakia,
Lichen planus, Lichenoid tissue reactions and
white sponge naevus.
• Management Stop the habit if possible.

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Vitiligo
• Etiopathogenesis autoimmune (loss of
melanocytes)
• Clinical features well-marginated cutaneous
milky white spots.
• Risk of ocular abnormalities, thyroid diseases,
Addison disease, pernicious anaemia and
diabetes mellitus
• Premature greying of the hair and alopecia
• Management Systemic or topical psoralen and
UVA (PUVA) therapy, Corticosteroids.
• Surgery for selected patients.

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