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RED LESIONS OF ORAL
MUCOSA
SOWMIYA L
I MDS
 Red lesions are a large, heterogeneous group
of disorders of the oral mucosa.
 Traumatic lesions, infections, developmental
anomalies, allergic reactions, immunologically
mediated diseases, premalignant lesions,
malignant neoplasm, and systemic diseases
are included in this group.
The red color of the lesions may be due to
 thin epithelium,
 inflammation,
 dilatation of blood vessels or increased
numbers of blood vessels,
 extravasation of blood into the oral soft tissues.
CLASSIFICATION
SOLITARY RED LESIONS
 TRAUMATIC ERYTHEMATOUS MACULES
AND EROSIONS
 PURPURIC MACULES
 INFLAMMATORY HYPERPLASIA
 REDDISH ULCERS
 NON PYOGENIC SOFT TISSUE
ODONTOGENIC INFECTION
 CHEMICAL OR THERMAL ERYTHEMATOUS
MACULE
 NICOTINE STOMATITIS
 ERYTHROPLAKIA, CARCINOMA IN SITU,
SQUAMOUS CELL CARCINOMA
 CANDIDIASIS
 MACULAR HEMANGIOMA AND
TELANGIECTASIA
 ALLERGIC MACULES
 HERALD LESION OF GENERALISED
STOMATITIS OR VESICULOBULLOUS
DISEASE
 METASTATIC TUMORS
 KAPOSI S SARCOMA
GENERALISED RED
CONDITIONS & MULTIPLE
ULCERS
 RECURRENT APHTHOUS STOMATITIS
 PRIMARY HERPETIC GINGIVOSTOMATITIS
 EROSIVE LICHEN PLANUS
 LICHENOID DRUG REACTION
 ERYTHEMA MULTIFORME
 ACUTE ATROPHIC CANDIDIASIS
 BENIGN MUCOUS MEMBRANE
PEMPHIGOID
 PEMPHIGUS
 CHRONIC ULCERATIVE STOMATITIS
 DESQUAMATIVE GINGIVITIS
 RADIATION AND CHEMOTHERAPY
MUCOSITIDES
 XEROSTOMIA
 PLASMA CELL GINGIVITIS
 STOMATITIS AREATA MIGRANS
 ALLERGIES
 POLYCYTHEMIA
 LUPUS ERYTHEMATOSUS
RED CONDITIONS OF THE
TONGUE
 MIGRATORY GLOSSITIS
 MEDIAN RHOMBOID GLOSSITIS
 DEFICIENCY STATES
 XEROSTOMIA
LOCALISED
INFLAMMATORY
LESIONS
ERYTHEMATOUS
CANDIDIASIS
 Erythematous candidiasis is a relatively
common form of candidiasis, with a high
incidence in HIV-infected patients and rarely in
patients receiving broad-spectrum antibiotics
or steroids.
 It may be acute or chronic.
 Etiology : Smoking , treatment with broad
spectrum antibiotics , steroids
 Also known as antibiotic sore mouth, Atrophic
oral candidiasis.
 Clinical features : Clinically, it is characterized
by erythematous patches or large areas,
usually located on the dorsum of the tongue
and palate.
 Not just reflect atrophy but increased
vascularization
 Diffuse borders distinguish it from erythroplakia
 Palate and dorsum of tongue are the sites
commonly affected.
 Burning sensation is a common symptom.
LAB DIAGNOSIS
 PAS staining – smear
 Swab culture
 Imprint culture technique
 Impression culture
 Salivary culture techniques
 Histopathologic examination
MANAGEMENT
 Identify the predisposing factor and eliminate it
 Proper denture hygiene
 Antifungals , topical and systemic
 Surgical excision of the lesion
ERYTHEMATOUS CANDIDIASIS
DEEP MYCOSIS
 Rare in the developed countries, except in HIV
disease and other immunocompromised
persons
 Histoplasmosis
 Cryptococcosis
 Blastomycosis
 Paracoccidiomycosis
HISTOPLASMOSIS
CRYPTOCOCCOSIS
BLASTOMYCOSIS
PARACOCCIDIOMYCOSIS
LICHEN PLANUS
 Etiology : The etiology of OLP is not known.
 Autoreactive T lymphocytes
 Stress
 Association of OLP with hepatitis C virus
LICHEN PLANUS
 Erythematous (atrophic) OLP is characterized
by a homogeneous red area.
 Present in the buccal mucosa or in the palate,
striae are frequently seen in the periphery.
 Some patients may display erythematous OLP
exclusively affecting attached gingiva. This
form of lesion may occur without any papules
or striae and presents as desquamative
gingivitis.
 Therefore, erythematous OLP requires a
histopathologic examination in order to arrive
at a correct diagnosis.
 Erythematous OLP of the gingiva exhibits a
similar clinical presentation as mucous
membrane pemphigoid.
 In pemphigoid lesions, the epithelium is easily
detached from the connective tissue by a
probe or a gentle searing force (Nikolsky’s
phenomenon).
 A biopsy for routine histology and direct
immunofluorescence are required for an
accurate differential diagnosis.
 Ulcerating conditions such as erythema
multiforme and adverse reactions to
nonsteroidal antiinflammatory drugs (NSAIDs)
may be difficult to distinguish from ulcerative
OLP.
 The former lesions, however, do not typically
appear with reticular or papular elements in
the periphery of the ulcerations.
HISTOPATHOLOGIC
FEATURES
 A saw-toothed appearance to the rete pegs,
 “liquefaction degeneration,” or necrosis of the
basal cell layer;
 an eosinophilic band may be seen just
beneath the basement membrane and
represent fibrin covering the lamina propria.
 A dense subepithelial band–shaped infiltrate of
lymphocytes and macrophages is also
characteristic of the disease.
Basal cell degeneration
Lymphotic
infiltration
MANAGEMENT
 sub- and supragingival plaque and calculus
removal
 steroid gels in prefabricated plastic trays may
be used for 30 minutes at each application to
increase the concentration of steroids in the
gingival tissue.
REITER S DISEASE
 Reiter s syndrome - Arthritis , urethritis,
mucocutaneous lesions and conjunctivitis
 Unknown etiology
 Clinical features
 Prevalent among adult men, between 20-30
yrs of age
 Urethritis may be the first sign of disease
 Arthritis is often bilateral and polyarticular
 Conjunctivitis is often mild
ORAL MANIFESTATIONS
 Painless, red, slightly elevated areas with a
white circinate border on the buccal mucosa,
lips and gingiva mistaken for aphthous ulcers
 Palatal lesions appear as small bright red
purpuric spots while lesions on the palate
resemble geographic tongue
HISTOLOGIC FEATURES
 Parakeratosis, acanthosis, neutrophil
infiltration of the epithelium occur
 Sometimes microabscess formation similar to
psoriasis occurs
 Treatment : disease undergoes spontaneous
regression , antibiotics and corticosteroids are
used.
REITER S DISEASE
GRAFT VERSUS HOST
DISEASE
 The major cause of GVHD is allogeneic
hematopoietic cell transplantation, also an
autologous transplantation may entail GVHD.
 In GVHD, it is the transplanted
immunocompetent tissue that attempts to
reject the tissue of the host.
 Recognition of alloantigens by donor T
lymphocytes
 Interaction between the recipient’s APCs and
the donor’s T lymphocytes
 Affects the entire GI system, including mouth
and skin and the liver.
 Oral lichenoid reactions as part of GVHD may
be seen both in acute and chronic GVHD.
 The clinical lichenoid reaction patterns are
indistinguishable from what is seen in patients
with OLP, that is, reticulum, erythema, and
ulcerations, but lichenoid reactions associated
with GVHD are typically associated with a
more widespread involvement of the oral
mucosa
 The skin lesions often present with pruritic
maculopapular and mobilliform rash, primarily
affecting the palms and soles.
 Violaceous scaly papules and plaques may
progress to a generalized erythroderma, bulla
formation, and, in severe cases, a toxic
epidermal necrolysis–like epidermal
desquamation.
 Diagnosis
 The presence of systemic GVHD facilitates the
diagnosis of oral mucosal changes of chronic
oral GVHD.
 In some instances, oral mucosa be the primary
or even the only site of chronic GVHD
involvement.
 It is not possible to distinguish between OLP
and oral GVHD based on clinical and
histopathologic features.
GVHD of tongue
BARTONELLA INFECTION
 Bacillary angiomatosis (BA) , also called
epithelioid angiomatosis, is a disease
characterized by unique vascular lesions
caused by infection with small, gram-negative
organisms of the genus Bartonella.
 Virtually all patients with this disease are
infected with HIV. BA occurs most frequently in
the later stages of HIV infection.
 Cutaneous BA is characterised by the
presence of lesions on or under the skin.
 papules or nodules which are red, globular
and non-blanching, with a vascular
appearance
 a purplish lichenoid plaque
 a subcutaneous nodule which may have
ulceration, similar to a bacterial abscess.
 While cutaneous BA is the most common form
of BA, BA can also affect several other parts of
the body, such as the brain, bone, bone
marrow, lymph nodes, gastrointestinal tract,
respiratory tract, spleen and liver.
 Symptoms vary depending on which parts of
the body is affected.
 The best method for diagnosis of cutaneous
BA remains biopsy with histopathologic study.
 Tissue specimens reveal a characteristic
vascular proliferation on routine hematoxylin &
eosin staining, in addition to numerous bacilli
demonstrable by modified silver staining or
electron microscopy.
 These organisms are not visualized following
staining for fungi or acid-fast mycobacteria;
staining with Brown-Brenn tissue Gram's stain
is also negative, which distinguishes
the Bartonella bacilli from most other small,
gram-negative rods.
BACILLARY ANGIOMATOSIS
REACTIVE LESIONS
PYOGENIC GRANULOMA
 RESPONSE OF THE TISSUE TO
NONSPECIFIC INFECTION
 It is a tumor like growth that is considered an
exaggerated conditioned response to minor
trauma
 Also called pregnancy tumor
 Etiology : calculus, food materials, and
overhanging dental restoration margins
 The prevalence of pregnancy epulides
increases toward the end of pregnancy (when
levels of circulating estrogens are highest),
and they tend to shrink after delivery (when
there is a precipitous drop in circulating
estrogens).
 This suggests that hormones play a role in the
etiology of the lesion, secondary to an
increase in angiogenic factor expression and a
reduction in the apoptosis of granulation
tissue.
 Both pyogenic granulomas and pregnancy
epulides may mature and become less
vascular and more collagenous, gradually
converting to fibrous epulides.
 They are composed of proliferating endothelial
tissue, much of which is canalized into a rich
vascular network with minimal collagenous
support. Neutrophils, as well as chronic
inflammatory cells, are consistently present
throughout the edematous stroma, with
microabscess formation.
 Histologically, differentiation from a
hemangioma is important.
MANAGEMENT
 The existence of these lesions indicates the
need for a periodontal consultation, and
treatment should include the elimination of
subgingival irritants and gingival pockets
throughout the mouth, as well as excision of
the gingival growth.
PYOGENIC GRANULOMA
PERIPHERAL GIANT CELL
GRANULOMA
 Peripheral giant cell granuloma or the so-
called “giant cell epulis” is the most common
oral giant cell lesion.
 It normally presents as a soft tissue purplish-
red nodule consisting of multinucleated giant
cells in a background of mononuclear stromal
cells and extravasated red blood cells.
 This lesion probably does not represent a true
neoplasm, but rather may be reactive in
nature, believed to be stimulated by local
irritation or trauma, but the cause is not
certainly known.
 ETIOLOGY : local irritation due to plaque or
calculus, poor dental restorations, ill fitting
dentures, dental extractions
 CLINICAL FEATURES : common in females
 Asymptomatic, rapid growth rate , occurs on
gingiva or alveolar process frequently anterior
to molars.
 It can be sessile or pedunculated
 Dark red, vascular in appearance commonly
exhibits surface ulceration.
HISTOLOGIC FEATURES
 Non encapsulated mass of tissue composed of a
delicate reticular and fibrillar connective tissue
stroma containing ovoid or spindle shaped young
connective tissue cella and multi nucleated giant
cells.
 Capillaries are numerous around the periphery of
the lesion
 Foci of hemorrhage with liberation of hemosiderin
pigment
 Spicules of newly formed osteoid or bone are
often found scattered through out the vascular
and cellular fibrous lesion.
Peripheral cuffing of bone
MANAGEMENT
 Conservative excision
 Recurrence rate is 10-15%
ATROPHIC
GEOGRAPHIC TONGUE
 Geographic tongue, also known as erythema
migrans ,ectopic geographic tongue or
erythema circinata migrans, benign migratory
glossitis, is a common benign hereditary
disorder of unknown etiology that primarily
affects the dorsal surface of the tongue.
 clinical features : Rarely, other areas of the
mucosa are also affected.
 Clinically it is often asymptomatic , patients
may complain of smarting sensation,
tenderness or a burning sensation, particularly
upon eating sour food.
 It manifests as circumferentially migrating and
leaves an erythematous area behind,
scattered, flat, irregular red lesions that are
often surrounded by a grey-yellowish
(keratotic) ring.
 Sometimes, it occurs in individuals with
psoriasis.
 Red areas extend, heal and are then replaced
by new lesions in other areas. Geographic
tongue sometimes affects patients with fissured
tongue (lingua plicata).
 Diagnosis/Histopathological features :
 In the peripheral region of erythema migrans,
characteristic histopathological features are:
hyperkeratosis, acanthosis and elongation of
the epithelial rete ridges.
 In the red portion of the lesion, localised loss of
filiform papillae is seen with epithelial atrophy
and mild subepithelial T lymphocyte infiltration.
 In addition, the epithelial surface is frequently
necrotic, and collections of neutrophils with
formation of microabscesses are observed
within the epithelium. Because these features
are reminiscent of psoriasis, this is called
a psoriasiform mucositis.
 Differential diagnosis :
 The histopathological appearance of mucosal
lesions in psoriasis pustulosa
generalisata and Reiter's syndrome cannot be
distinguished from erythema migrans.
 It may also be mistaken for lichen planus.
GEOGRAPHIC TONGUE
LUPUS ERYTHEMATOSUS
 Definition : Lupus erythematosus is a chronic
immunologically mediated disease.
 Etiology : Autoimmune. the main feature is the
formation of antibodies to DNA, which may
initiate immune complex reactions, in
particular a vasculitis.
 Clinical features : Two main forms of the
disease are recognized: discoid (DLE)
and systemic (SLE). Oral lesions develop in
15–25% of cases in DLE and in 30–45% of
cases in SLE, usually in association with
 Three subtypes of lupus-specific skin lesions
have been described: acute, subacute, and
chronic.
 Acute cutaneous lupus occurs in 30 to 50% of
patients and is classically represented by the
butterfly rash–mask-shaped erythematous
eruption involving the malar areas and bridge
of the nose but typically (as opposed to
dermatomyositis [DM]) sparing nasolabial
folds.
 Bullous lupus and localized erythematous
 Subacute lupus – cutaneous , non indurated
psoriasiform annulay polycyclic lesions that
resolve without scaring , although occasionally
with post inflammatory dyspigmentation
 Chronic cutaneous lupus – classic discoid rash
localised or generalised, hypertrophic lupus in
verrucous form, mucosal lupus, lichen planus
overlap
 The oral lesions are characterized by a well-
defined central atrophic red area surrounded
by a sharp elevated border of
irradiating whitish striae, brush border
appearance.
 Telangiectasia, petechiae, edema, erosions,
ulcerations, and white hyperkeratotic plaques
may be seen.
 Buccal mucosa, gingiva, and labial mucosa
are the most commonly affected intraoral sites.
Isolated erythematous areas are also
common, especially on the palate.
 Differential diagnosis : Lichen planus,
geographic glossitis, speckled leukoplakia,
erythroplakia, cicatricial pemphigoid, syphilis.
 Treatment : Steroids, Nonsteroidal anti-
inflammatory drugs (nsaids) are frequently used in
SLE for symptomatic relief of arthritis but are of
little benefit in more severe disease.
 Cyclosporine, tacrolimus, sirolimus, methotrexate,
and intravenous immunoglobulins have also been
used in SLE. Antimalarials, such as
hydroxychloroquine, are effective in cutaneous
lupus with fewer adverse effects.
ERYTHROPLAKIA
 Definition : Erythroplakia, or Queyrat
erythroplasia, is a premalignant lesion that
rarely occurs on the oral mucosa.
 It is defined as a red patch or plaque that
cannot be classified clinically or pathologically
under any other condition.
 Etiology : Unknown ( smoking and alcohol
abuse are important risk factors )
 Clinical features : It appears as a usually
asymptomatic, fiery red, well demarcated
plaque, with a smooth and velvety surface.
 The red lesions may be associated with white
spots or small plaques. The floor of the mouth,
retromolar area, soft palate, and tongue are the
most common sites of involvement.
Homogeneous erythroplakia
Erythroplakia interspersed with patches of
leukoplakia
Granular or speckled erythroplakia
 Erythroplakia occurs more frequently between
the ages of 50 and 70 years. Over 91% of
erythroplakia s histologically demonstrate
severe dysplasia, carcinoma in situ, or early
invasive squamous-cell carcinoma at the time
of diagnosis.
 Laboratory tests : Histopathological
examination.
 Differential diagnosis : Erythematous
candidiasis, lichen planus, early squamous-cell
carcinoma, local irritation.
 Treatment : cold knife Surgical excision laser
surgery.
ERYTHROPLAKIA –
SPECKLED
THERMAL BURN
 Definition and etiology : Thermal burns to
the oral mucosa are fairly common, usually
due to contact with very hot foods, liquids, or
hot metal objects.
 Clinical features : Clinically, the condition
appears as a red, painful erythema that may
undergo desquamation, leaving erosions.
 The lesions heal spontaneously in about a
week. The diagnosis is made exclusively on
clinical grounds.
 Differential diagnosis : Chemical burn,
traumatic lesions, herpes simplex, aphthous
ulcers, drug reactions.
 Treatment : No treatment is required.
DRUGS AND CHEMICAL BURN
 Aspirin tablets/powder
 Tooth ache drops containing creosote,
guaiacol, phenol derivatives
 Dental medicaments such as chromic acid,
trichloroacetic acid, silver nitrate, beechwood
creosote, eugenol, paraformaldehyde, ticture
of iodine
DRUGS
 Erythema multiforme – antibiotics like
sulfonamides, tetracyclines, amoxicillin,
ampicillin. Anticonvulsants – phenytoin,
barbiturates
 Stevenson johnson syndrome –
acetaminophen and NSAID s
THERMAL BURN
AVITAMINOSIS B12
 Avitaminosis is any disease caused by
chronic or long-term vitamin deficiency or
caused by a defect in metabolic conversion,
such as tryptophan to niacin. They are
designated by the same letter as the vitamin
 Avitaminosis B12 causes pernicious anemia
 The clinical symptoms are weakness, fatigue,
shortness of breath and neurologic
abnormalities.
 The presence of oral signs and symptoms,
include glossitis, angular cheilitis, recurrent
oral ulcer, oral candidiasis, diffuse
erythematous mucositis and pale oral mucosa.
 Management is through vitamin supplements
VITAMIN B COMPLEX
 Vitamin B1 (thiamine)
 Vitamin B2 (riboflavin)
 Vitamin B3 (niacin or nicotinic acid)
 Vitamin B5 (Pantothenic acid)
 Vitamin B6 (pyridoxine, pyridoxal, pyridoxamine)
 Vitamin B7 (biotin)
 Vitamin B9 (folic acid)
 Vitamin B12 (various cobalamins;
commonly cyanocobalamin or methylcobalamin in
vitamin supplements)
VITAMIN B12 DEFICIENCY
SESSION 2
PURPURA
 Purpura is a condition of red or purple
discolored spots on the skin that do
not blanch on applying pressure.
 The spots are caused by bleeding underneath
the skin usually secondary to vasculitis.
 They measure 0.3–1 cm (3–10 mm),
whereas petechiae measure less than 3 mm,
and ecchymoses greater than 1 cm
 Purpura are a common and nonspecific
medical sign.
 Platelet disorders (thrombocytopenic purpura)
 Primary thrombocytopenic purpura
 Secondary thrombocytopenic purpura
 Post-transfusion purpura
 Vascular disorders (nonthrombocytopenic
purpura)
 Microvascular injury, as seen in senile (old age)
purpura, when blood vessels are more easily
damaged
 Hypertensive states
 Deficient vascular support
 Vasculitis, as in the case of Henoch-Schönlein
purpura
 Coagulation disorders - Disseminated
intravascular coagulation (DIC)
 Scurvy (vitamin C deficiency) - defect in
collagen synthesis which results in weakened
capillary walls and cells
PURPURA
IDIOPATHIC THROMBOCYTOPENIC
PURPURA
 Definition Thrombocytopenic purpura is a
hematological disorder characterized by a
decrease in platelets in the peripheral blood.
 Etiology Presumably a nonspecific viral
infection, myelotoxic agents.
 Clinical features The oral manifestations
consist of red lesions in the form of petechiae,
ecchymoses, or even hematomas, usually
located on the palate and buccal mucosa.
 Spontaneous gingival bleeding is a constant
early finding.
 Purpuric skin rash, epistaxis, and bleeding
from the gastrointestinal and urinary tract are
common.
 Laboratory tests Peripheral platelet count,
bone-marrow aspiration, bleeding and clotting
times.
 Differential diagnosis Aplastic anemia,
leukemias, polycythemia vera,
agranulocytosis, drug reactions.
 Treatment Steroids, platelet transfusions,
cessation of drug treatment if it is drug-related.
VASCULAR
TELANGECTASIA
 Persistent dilatation of small, superficial blood
vessels; rarely inherited
 They are red seldom over 5mm in diameter
and blanch readily on digital pressure, which
easily differentiates them from red petechiae.
 They may occur as red solitary lesions or
multiple lesions.
 The uncommon Osler-Weber-Rendu
syndrome (hereditary haemorrhagic
teleangiectasia; HHT) is inherited via an
autosomal dominant trait, however, family
history can be negative.
 Clinically, oral and peri-oral telangiectasias are
observed, as well as telangiectasias in the
nose, the gastro-intestinal tract and on the
palms of the hands. They may bleed which
may cause chronic iron-deficiency anaemia.
OSLER WEBER RENDU
SYNDROME
SCLERODERMA
 Scleroderma is a rare autoimmune disorder of
blood vessels and connective tissue, which is
divided into a progressive systemic and a
localised form (circumscribed scleroderma).
 The disease most commonly affects adult
middle-aged females. In later stages,
development of a mask-like face with restricted
mouth opening (microstomia), telangiectasias,
smooth tongue surface and shortened lingual
frenum.
SCLERODERMA
CREST SYNDROME
 A relatively mild variant is characterised by
subcutaneous calcification (CREST syndrome:
calcinosis cutis, Raynaud's phenomenon,
esophageal dysfunction, sclerodactyly and
telangiectasia); frequent association with
Sjögren's syndrome.
CREST SYNDROME
 Differential diagnosis
 Oral lesions in Osler-Weber-Rendu syndrome:
scleroderma, chronic liver diseases, post-
irradiation state
 Oral lesions in scleroderma: Osler-Weber-
Rendu syndrome, oral submucous fibrosis,
secondary Sjögren's syndrome
 Treatment and prognosis
 Osler-Weber-Rendu syndrome: local
haemostasis (cryo-surgery or laser), treatment
of anaemia.
 Scleroderma: management is difficult;
enhancement of micro-circulation ,
corticosteroids, in some cases
immunosuppressants. Prognosis is dependent
on type of disease; from favourable to poor
and lethal.
ANGIOMA
 Developmental vascular malformation
(hamartoma) or benign vascular tumour. Two
types - cavernous and capillary types.
 In the oral cavity, the most common
mesenchymal tumour of infancy.
 Commonest localisation: tongue, lips, buccal
mucosa.
 Capillary hemangiomas are further classified into
juvenile , senile , nevus flammeus
 Juvenile hemangioma
 Most common type of capillary hemangioma
 Majority occur in head and neck region shortly
after birth
 Period of rapid growth then begin to regress after
about a year
 Fully developed hemangioma is elevated,
lobulated, sharply circumscribed, and bright red
 They require no treatment.
STRAWBERRY HEMANGIOMA
 Senile hemangioma
 Start appearing in early adulthood, and the
number of lesion increases with age.
 The lesions are bright red and vary in dia from
1mm to several mm s.
 The larger lesions are soft and dome shaped.
CHERRY HEMANGIOMA
 Nevus flammeus
 Also known as port wine stains, are present at
birth are unilateral and located on face and
neck
 Sharply circumscribed and range from small
red macules to large red flat patches that are
blanched by pressure.
 Haemangiomatous vascular malformation of
the face related to maxillary division of the
trigeminal nerve (port wine stain) and
involvement of the leptomeninges occur
in Sturge-Weber syndrome
 Complications: epilepsy, contralateral
hemiplegia (rare), mental retardation
(common).
ANGIOMAS
 Angiomatous syndromes
 Osler- Weber-Rendu syndrome (hereditary
hemorrhagic telangiectasia)
 blue rubber bleb nevus syndrome
 Bannayan-Zonana
 Sturge-Weber
 Klippel-Trénaunay syndrome
 Servelle-Martorell syndrome
 von Hippel-Lindau syndrome
 Maffucci’s syndrome
HEMANGIOMA
CAVERNOUS HEMANGIOMA
ANGIOKERATOMAFABRY S DIASEASE
 Angiokeratoma is a benign cutaneous lesion
of capillaries, resulting in small marks of red to
blue color and characterized by
hyperkeratosis.
 Angiokeratoma corporis diffusum refers
to Fabry's disease is a rare genetic lysosomal
storage disease, inherited in an X-
linked manner. Fabry disease can cause a
wide range of systemic symptoms. It is a form
of sphingolipidosis, as it involves dysfunctional
metabolism of sphingolipids.
 Clinical features – dermatological
manifeatations – Angiokeratomas occur
commonly on the thighs, lower abdomen, and
groin)
 Anhidrosis (lack of sweating) is a common
symptom, and less
commonly hyperhidrosis (excessive sweating).
 Ocular involvement may be present
showing cornea verticillata (also known as
vortex keratopathy), i.e. clouding of the
corneas. This clouding does not affect vision.
HISTOPATHOLOGY
 Angiokeratomas characteristically have large
dilated blood vessels in the
superficial dermis and hyperkeratosis (overlyin
g the dilated vessels).
NEOPLASMS
SQUAMOUS CARCINOMA
 The early stage of squamous-cell carcinoma
may present as an asymptomatic, atypical red
patch.
 The clinical features are identical to
erythroplakia, erythematous candidiasis, or
contact reactions to dental materials.
 In these cases, a biopsy should be taken to
allow a conclusive diagnosis.
KAPOSIS SARCOMA
 Malignant neoplasm composed of spindle cells
and vascular elements
 Occurs in homosexual men affected with AIDS
commonly
 Classic , Endemic and epidemic types
 Classic or sporadic type – commonly occurs in
older persons of jewish origin, involves the
skin of lower extremities
 Oral mucosal involvement is rare in this
 Endemic form – occurs in native black
population
 Epidemic form affects those with HIV and
other immunological disorder
 Lesions widely distributed over the skin
 Mucosa and lymph nodes are involved and
response to treatment is poor
 KS can involve any oral site but most
frequently involves the attached mucosa of the
palate, gingiva, and dorsum of the tongue.
 Lesions begin as blue purple or red purple flat
discolorations that can progress to tissue
masses that may ulcerate.
 The lesions do not blanch with pressure. Initial
lesions are asymptomatic but can cause
discomfort and interfere with speech, denture
use, and eating when lesions progress.
 The differential diagnosis includes
ecchymosis, vascular lesions, and salivary
gland tumors.
 Definitive diagnosis requires biopsy. Because
KS is a multicentric neoplastic disease,
multiple sites of involvement can occur,
including skin, lymph nodes, gastrointestinal
tract, and other organ systems.
TREATMENT
 Surgical excision, electrocautery and radiation
therapy.
 Patients with disseminated disease may be
treated with immunomodulators and single
agent or combination chemotherapy.
WEGENER S
GRANULOMATOSIS
 Granulomatosis with polyangiitis (GPA),
formerly referred to as Wegener's
granulomatosis (WG), is a systemic disorder
that involves both
granulomatosis and polyangiitis.
 It is a form of vasculitis (inflammation of blood
vessels) that affects small- and medium-size
vessels in many organs
 Oral cavity: strawberry gingivitis, underlying
bone destruction with loosening of teeth, non-
specific ulcerations throughout oral mucosa
MIDLINE LETHAL
GRANULOMA
 Lethal midline granuloma is a condition
affecting the nose and palate.
 Macroscopically the lesions usually look like
necrotic granulomas and are characterized by
ulceration and destruction of the nose and
paranasal sinuses with erosion of soft tissues,
bone and cartilage of the region.
 The patients show an aggressive and lethal
course with rapid destruction of the nose and
face (midline), therefore the term “lethal
midline granuloma”.
 This disease occurs around the fourth decade
and occurs commonly in males.
 The major symptoms are nasal stuffiness with
or without nasal discharge.
 Oral or nasal ulcer with conjunctivitis may also
occur. Perforation of the nasal septum with
mutilation of the surrounding tissues
eventually occurs.
 Morphologically it is characterized by
extensive ulceration of mucosal sites with a
lymphomatous infiltrate that is diffuse, but has
an angiocentric and angiodestructive growth
pattern.
GENERALISED
DENTURE STOMATITIS
 Definition : Denture stomatitis, or denture
sore mouth, is a frequent condition in patients
who wear dentures continuously for extended
times.
 Etiology : Mechanical irritation from
dentures, Candida albicans, or a tissue
response to microorganisms living beneath the
dentures.
 Also caused by bacteria such as
streptococcus, veillonella, lactobacillus,
prevotella and actinomyces.
 Clinical features : The condition is
characterized by diffuse erythema, edema, and
sometimes petechiae and white spots that
represent accumulations of candidal hyphae,
almost always located in the denture bearing
area of the maxilla.
 The condition is usually asymptomatic. The
diagnosis is based on clinical criteria.
 Type I – localised to minor erythematous areas
caused by trauma from denture
 Type II – affects major part of denture covered
mucosa
 Type III – granular mucosa in the central part of
the palate
 Differential diagnosis : Allergic contact
stomatitis due to acrylic.
 Treatment : Improvement of denture fit, proper
oral hygiene, and topical antimycotics.
DENTURE STOMATITIS
MEDIAN RHOMBOID GLOSSITIS
 Definition : Median rhomboid glossitis is a
rare condition that occurs exclusively on the
dorsum of the tongue.
 Etiology : Presumably developmental,
Candida albicans , bacteria may also be
involved.
 Clinical features : It presents as a well-
demarcated erythematous rhomboid area,
 along the midline of the dorsum of the tongue,
immediately anterior to the circumvallate
papillae.
 The surface of the lesion may be smooth or
lobulated. Atrophy of filiform papillae.
 Differential diagnosis : Candidiasis,
lymphangioma, geographic tongue, syphilis,
hemangioma.
 Treatment : No treatment is required.
KISSING LESIONS
 A concurrent erythematous lesion may be
observed in the palatal mucosa and it is called
kissing lesion.
 Management is restricted to a reduction in
predisposing factors.
KISSING LESION ON THE
PALATE
MEDIAN RHOMBOID GLOSSITIS
RADIATION MUCOSITIS
 Definition and etiology : Oral radiation
mucositis is a side effect of radiation treatment
of head and neck tumors.
 Clinical features : The oral lesions are
classified as early and late. Early reactions
may begin at the end of the first week of
radiotherapy, and consist of erythema and
edema of the oral mucosa.
 Soon after, erosions or ulcers may develop,
covered by a whitish-yellow exudate.
 Xerostomia, loss of taste, and burning and pain
during mastication, swallowing, and speech are
common. The diagnosis is made clinically.
 Differential diagnosis : Mucositis due to
chemotherapy, graft-versushost disease,
erythema multiforme, herpetic stomatitis, lichen
planus.
 Treatment : Supportive treatment. Cessation
of the radiation treatment, B-complex vitamins,
and sometimes low doses of steroids are
indicated.
RADIATION MUCOSITIS
POLYCYTHEMIA
 Also called erythremia is chronic and
sustained elevation in the number of
erythrocytes and level of hemoglobin.
 Primary
 secondary
 Primary – polycythemia vera is a neoplastic
condition of erythropoietic sysyem
 Secondary – is a sustained elevation of
erythrocytes and hemoglobin usually resulting
from bone marrow stimulation caused by living
at high altitude or chronic pulmonary disease
such as emphysema
 The entire oral mucosa of patients with
polycythemia has a deep red or purple color.
 Soft palate and gingiva are prone to easy
bleeding and petechial hemorrhages may be
seen on the palate and labial mucosa
 Infarcts may occur in the smaller blood vessel
leading to ulcers
DIAGNOSIS
 Increase in erythrocytes
 Hemoglobin concentration
 hematocrit
PLASMA CELL GINGIVITIS
 Definition : Plasma-cell gingivitis is a rare and
unique gingival disorder, characterized
histopathologically by a dense chronic
inflammatory infiltration of the lamina propria,
mainly of plasma cells.
 Etiology : Unknown. Reactions to local
allergens, chronic infections, and plasma-cell
dyscrasias have been considered as possible
causes.
 Clinical features : Clinically, both free and
attached gingiva are bright red and edematous,
with a loss of normal stippling. The gingivitis
may be localized or widespread, and is
frequently accompanied by a burning
sensation.
 Rarely, similar lesions may be seen on the
tongue and lips.
 Ulcers , epithelial sloughing and desquamation
may be present.
 Patient may complain of pain, sensitivity and
bleeding of gingiva during brushing.
 Laboratory tests : patch testing to identify the
allergen, Histopathological and histochemical
examination, immunofluorescence.
 Histopathology : parakeratosis , epithelial
hyperplasia , dense infiltrate of plasma cells in
the lamina propria , dilated blood capillaries.
 Differential diagnosis : Desquamative
gingivitis, erosive lichen planus,
vesiculobullous disorders.
 Pubertal or pregnancy induced gingivitis,
plaque associated gingivitis.
 Rapid onset - PCS.
 Treatment : Remove the allergen if possible.
Pain control, Topical or systemic steroids.
 Gingivectomies to recontour lesions that are
long standing and fibrotic.
PLASMA CELL GINGIVITIS
PEMPHIGUS
PEMPHIGOID
ERYTHEMA MULTIFORME
 EM is an acute, self-limited, inflammatory
mucocutaneous disease that manifests on the
skin and often oral mucosa, although other
mucosal surfaces, such as the genitalia, may
also be involved.
 EM is classified as E M minor if there is less
than 10% of skin involvement and there is
minimal to no mucous membrane involvement,
whereas EM major has more extensive but still
characteristic skin involvement, with the oral
mucosa and other mucous membranes
affected.
 Historically, fulminant forms of EM were
labeled Stevens- Johnson syndrome (SJS)
and toxic epidermal necrolysis [TEN (Lyell
disease)].
ETIOLOGY
 EM is a hypersensitivity reaction, and the most
common inciting factors are infection,
particularly with HSV, or drug reactions to
NSAIDS or anticonvulsants.
 Other viral, bacterial, fungal, and protozoal
infections and medications may also play a
role.
CLINICAL FEATURES
 EM generally affects those between ages 20
and 40 years, with 20% occurring in children.
 There is often a prodrome of fever, malaise,
headache, sore throat, rhinorrhea, and cough.
 Skin lesions begin as red macules that
become papular, starting primarily in the hands
and moving centripetally toward the trunk in a
symmetric distribution. The most common
sites of involvement are the upper extremities,
face, and neck.
 The skin lesions may take several forms—
hence the term multiforme - irregular bullae,
erosions, or ulcers surrounded by extensive
areas of inflammation, Severe crusting and
bleeding of the lips are common.
 The classic skin lesion consists of a central
blister or necrosis with concentric rings of
variable color around it called typical “target”
or “iris” lesion that is pathognomonic of EM;
variants are called “atypical target” lesions .
ORAL MANIFESTATIONS
 mild erythema and erosion to painful
ulcerations.
 When severe, ulcers may be large and
confluent, causing difficulty in eating, drinking,
and swallowing, and patients with severe EM
may drool blood-tinged saliva.
 Differential diagnosis : Primary HSV
gingivostomatitis, Autoimmune vesiculobullous
disease such as pemphigus and pemphigoid,
recurrent aphthous ulcers.
 Management : systemic or topical analgesics,
corticosteroids, antiviral medication,
azathioprine and dapsone , antimalarials
prevents recurrence.
REFERENCES
 Peripheral giant cell granuloma Padam
Narayan Tandon, S. K. Gupta,1 Durga Shanker
Gupta, Sunit Kumar Jurel,2 and Abhishek
Saraswat
 Oral Manifestations of Vitamin B12 Deficiency:
A Case Report Hélder Antônio Rebelo Pontes,
DDS, MSc, PhD; Nicolau Conte Neto, DDS;
Karen Bechara Ferreira, DDS; Felipe Paiva
Fonseca; Gizelle Monteiro Vallinoto; Flávia
Sirotheau Corrêa Pontes, DDS, MSc, PhD;
Décio dos Santos Pinto Jr, DDS, MSc, PhD
 Text book of Burket s oral medicine
 Text book of Differential Diagnosis of oral and
maxillofacial lesions by Norman K Wood and
Paul W Goaz
 Shafer s text book of oral pathology

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RED LESIONS

  • 1. RED LESIONS OF ORAL MUCOSA SOWMIYA L I MDS
  • 2.  Red lesions are a large, heterogeneous group of disorders of the oral mucosa.  Traumatic lesions, infections, developmental anomalies, allergic reactions, immunologically mediated diseases, premalignant lesions, malignant neoplasm, and systemic diseases are included in this group.
  • 3. The red color of the lesions may be due to  thin epithelium,  inflammation,  dilatation of blood vessels or increased numbers of blood vessels,  extravasation of blood into the oral soft tissues.
  • 5.
  • 6.
  • 7. SOLITARY RED LESIONS  TRAUMATIC ERYTHEMATOUS MACULES AND EROSIONS  PURPURIC MACULES  INFLAMMATORY HYPERPLASIA  REDDISH ULCERS  NON PYOGENIC SOFT TISSUE ODONTOGENIC INFECTION  CHEMICAL OR THERMAL ERYTHEMATOUS MACULE  NICOTINE STOMATITIS
  • 8.  ERYTHROPLAKIA, CARCINOMA IN SITU, SQUAMOUS CELL CARCINOMA  CANDIDIASIS  MACULAR HEMANGIOMA AND TELANGIECTASIA  ALLERGIC MACULES  HERALD LESION OF GENERALISED STOMATITIS OR VESICULOBULLOUS DISEASE  METASTATIC TUMORS  KAPOSI S SARCOMA
  • 9. GENERALISED RED CONDITIONS & MULTIPLE ULCERS  RECURRENT APHTHOUS STOMATITIS  PRIMARY HERPETIC GINGIVOSTOMATITIS  EROSIVE LICHEN PLANUS  LICHENOID DRUG REACTION  ERYTHEMA MULTIFORME  ACUTE ATROPHIC CANDIDIASIS  BENIGN MUCOUS MEMBRANE PEMPHIGOID  PEMPHIGUS  CHRONIC ULCERATIVE STOMATITIS
  • 10.  DESQUAMATIVE GINGIVITIS  RADIATION AND CHEMOTHERAPY MUCOSITIDES  XEROSTOMIA  PLASMA CELL GINGIVITIS  STOMATITIS AREATA MIGRANS  ALLERGIES  POLYCYTHEMIA  LUPUS ERYTHEMATOSUS
  • 11. RED CONDITIONS OF THE TONGUE  MIGRATORY GLOSSITIS  MEDIAN RHOMBOID GLOSSITIS  DEFICIENCY STATES  XEROSTOMIA
  • 13. ERYTHEMATOUS CANDIDIASIS  Erythematous candidiasis is a relatively common form of candidiasis, with a high incidence in HIV-infected patients and rarely in patients receiving broad-spectrum antibiotics or steroids.  It may be acute or chronic.
  • 14.  Etiology : Smoking , treatment with broad spectrum antibiotics , steroids  Also known as antibiotic sore mouth, Atrophic oral candidiasis.
  • 15.  Clinical features : Clinically, it is characterized by erythematous patches or large areas, usually located on the dorsum of the tongue and palate.  Not just reflect atrophy but increased vascularization  Diffuse borders distinguish it from erythroplakia  Palate and dorsum of tongue are the sites commonly affected.  Burning sensation is a common symptom.
  • 16. LAB DIAGNOSIS  PAS staining – smear  Swab culture  Imprint culture technique  Impression culture  Salivary culture techniques  Histopathologic examination
  • 17. MANAGEMENT  Identify the predisposing factor and eliminate it  Proper denture hygiene  Antifungals , topical and systemic  Surgical excision of the lesion
  • 18.
  • 20. DEEP MYCOSIS  Rare in the developed countries, except in HIV disease and other immunocompromised persons  Histoplasmosis  Cryptococcosis  Blastomycosis  Paracoccidiomycosis
  • 25. LICHEN PLANUS  Etiology : The etiology of OLP is not known.  Autoreactive T lymphocytes  Stress  Association of OLP with hepatitis C virus
  • 26. LICHEN PLANUS  Erythematous (atrophic) OLP is characterized by a homogeneous red area.  Present in the buccal mucosa or in the palate, striae are frequently seen in the periphery.  Some patients may display erythematous OLP exclusively affecting attached gingiva. This form of lesion may occur without any papules or striae and presents as desquamative gingivitis.  Therefore, erythematous OLP requires a histopathologic examination in order to arrive at a correct diagnosis.
  • 27.  Erythematous OLP of the gingiva exhibits a similar clinical presentation as mucous membrane pemphigoid.  In pemphigoid lesions, the epithelium is easily detached from the connective tissue by a probe or a gentle searing force (Nikolsky’s phenomenon).  A biopsy for routine histology and direct immunofluorescence are required for an accurate differential diagnosis.
  • 28.  Ulcerating conditions such as erythema multiforme and adverse reactions to nonsteroidal antiinflammatory drugs (NSAIDs) may be difficult to distinguish from ulcerative OLP.  The former lesions, however, do not typically appear with reticular or papular elements in the periphery of the ulcerations.
  • 29. HISTOPATHOLOGIC FEATURES  A saw-toothed appearance to the rete pegs,  “liquefaction degeneration,” or necrosis of the basal cell layer;  an eosinophilic band may be seen just beneath the basement membrane and represent fibrin covering the lamina propria.  A dense subepithelial band–shaped infiltrate of lymphocytes and macrophages is also characteristic of the disease.
  • 31. MANAGEMENT  sub- and supragingival plaque and calculus removal  steroid gels in prefabricated plastic trays may be used for 30 minutes at each application to increase the concentration of steroids in the gingival tissue.
  • 32.
  • 33. REITER S DISEASE  Reiter s syndrome - Arthritis , urethritis, mucocutaneous lesions and conjunctivitis  Unknown etiology  Clinical features  Prevalent among adult men, between 20-30 yrs of age  Urethritis may be the first sign of disease  Arthritis is often bilateral and polyarticular  Conjunctivitis is often mild
  • 34. ORAL MANIFESTATIONS  Painless, red, slightly elevated areas with a white circinate border on the buccal mucosa, lips and gingiva mistaken for aphthous ulcers  Palatal lesions appear as small bright red purpuric spots while lesions on the palate resemble geographic tongue
  • 35. HISTOLOGIC FEATURES  Parakeratosis, acanthosis, neutrophil infiltration of the epithelium occur  Sometimes microabscess formation similar to psoriasis occurs  Treatment : disease undergoes spontaneous regression , antibiotics and corticosteroids are used.
  • 37. GRAFT VERSUS HOST DISEASE  The major cause of GVHD is allogeneic hematopoietic cell transplantation, also an autologous transplantation may entail GVHD.  In GVHD, it is the transplanted immunocompetent tissue that attempts to reject the tissue of the host.  Recognition of alloantigens by donor T lymphocytes  Interaction between the recipient’s APCs and the donor’s T lymphocytes
  • 38.  Affects the entire GI system, including mouth and skin and the liver.  Oral lichenoid reactions as part of GVHD may be seen both in acute and chronic GVHD.  The clinical lichenoid reaction patterns are indistinguishable from what is seen in patients with OLP, that is, reticulum, erythema, and ulcerations, but lichenoid reactions associated with GVHD are typically associated with a more widespread involvement of the oral mucosa
  • 39.  The skin lesions often present with pruritic maculopapular and mobilliform rash, primarily affecting the palms and soles.  Violaceous scaly papules and plaques may progress to a generalized erythroderma, bulla formation, and, in severe cases, a toxic epidermal necrolysis–like epidermal desquamation.
  • 40.  Diagnosis  The presence of systemic GVHD facilitates the diagnosis of oral mucosal changes of chronic oral GVHD.  In some instances, oral mucosa be the primary or even the only site of chronic GVHD involvement.  It is not possible to distinguish between OLP and oral GVHD based on clinical and histopathologic features.
  • 42. BARTONELLA INFECTION  Bacillary angiomatosis (BA) , also called epithelioid angiomatosis, is a disease characterized by unique vascular lesions caused by infection with small, gram-negative organisms of the genus Bartonella.  Virtually all patients with this disease are infected with HIV. BA occurs most frequently in the later stages of HIV infection.
  • 43.  Cutaneous BA is characterised by the presence of lesions on or under the skin.  papules or nodules which are red, globular and non-blanching, with a vascular appearance  a purplish lichenoid plaque  a subcutaneous nodule which may have ulceration, similar to a bacterial abscess.
  • 44.  While cutaneous BA is the most common form of BA, BA can also affect several other parts of the body, such as the brain, bone, bone marrow, lymph nodes, gastrointestinal tract, respiratory tract, spleen and liver.  Symptoms vary depending on which parts of the body is affected.
  • 45.  The best method for diagnosis of cutaneous BA remains biopsy with histopathologic study.  Tissue specimens reveal a characteristic vascular proliferation on routine hematoxylin & eosin staining, in addition to numerous bacilli demonstrable by modified silver staining or electron microscopy.
  • 46.  These organisms are not visualized following staining for fungi or acid-fast mycobacteria; staining with Brown-Brenn tissue Gram's stain is also negative, which distinguishes the Bartonella bacilli from most other small, gram-negative rods.
  • 49. PYOGENIC GRANULOMA  RESPONSE OF THE TISSUE TO NONSPECIFIC INFECTION  It is a tumor like growth that is considered an exaggerated conditioned response to minor trauma  Also called pregnancy tumor  Etiology : calculus, food materials, and overhanging dental restoration margins
  • 50.  The prevalence of pregnancy epulides increases toward the end of pregnancy (when levels of circulating estrogens are highest), and they tend to shrink after delivery (when there is a precipitous drop in circulating estrogens).  This suggests that hormones play a role in the etiology of the lesion, secondary to an increase in angiogenic factor expression and a reduction in the apoptosis of granulation tissue.
  • 51.  Both pyogenic granulomas and pregnancy epulides may mature and become less vascular and more collagenous, gradually converting to fibrous epulides.
  • 52.  They are composed of proliferating endothelial tissue, much of which is canalized into a rich vascular network with minimal collagenous support. Neutrophils, as well as chronic inflammatory cells, are consistently present throughout the edematous stroma, with microabscess formation.  Histologically, differentiation from a hemangioma is important.
  • 53. MANAGEMENT  The existence of these lesions indicates the need for a periodontal consultation, and treatment should include the elimination of subgingival irritants and gingival pockets throughout the mouth, as well as excision of the gingival growth.
  • 55.
  • 56. PERIPHERAL GIANT CELL GRANULOMA  Peripheral giant cell granuloma or the so- called “giant cell epulis” is the most common oral giant cell lesion.  It normally presents as a soft tissue purplish- red nodule consisting of multinucleated giant cells in a background of mononuclear stromal cells and extravasated red blood cells.  This lesion probably does not represent a true neoplasm, but rather may be reactive in nature, believed to be stimulated by local irritation or trauma, but the cause is not certainly known.
  • 57.  ETIOLOGY : local irritation due to plaque or calculus, poor dental restorations, ill fitting dentures, dental extractions  CLINICAL FEATURES : common in females  Asymptomatic, rapid growth rate , occurs on gingiva or alveolar process frequently anterior to molars.  It can be sessile or pedunculated  Dark red, vascular in appearance commonly exhibits surface ulceration.
  • 58. HISTOLOGIC FEATURES  Non encapsulated mass of tissue composed of a delicate reticular and fibrillar connective tissue stroma containing ovoid or spindle shaped young connective tissue cella and multi nucleated giant cells.  Capillaries are numerous around the periphery of the lesion  Foci of hemorrhage with liberation of hemosiderin pigment  Spicules of newly formed osteoid or bone are often found scattered through out the vascular and cellular fibrous lesion.
  • 59.
  • 61.
  • 62. MANAGEMENT  Conservative excision  Recurrence rate is 10-15%
  • 64. GEOGRAPHIC TONGUE  Geographic tongue, also known as erythema migrans ,ectopic geographic tongue or erythema circinata migrans, benign migratory glossitis, is a common benign hereditary disorder of unknown etiology that primarily affects the dorsal surface of the tongue.  clinical features : Rarely, other areas of the mucosa are also affected.
  • 65.  Clinically it is often asymptomatic , patients may complain of smarting sensation, tenderness or a burning sensation, particularly upon eating sour food.  It manifests as circumferentially migrating and leaves an erythematous area behind, scattered, flat, irregular red lesions that are often surrounded by a grey-yellowish (keratotic) ring.  Sometimes, it occurs in individuals with psoriasis.
  • 66.  Red areas extend, heal and are then replaced by new lesions in other areas. Geographic tongue sometimes affects patients with fissured tongue (lingua plicata).  Diagnosis/Histopathological features :  In the peripheral region of erythema migrans, characteristic histopathological features are: hyperkeratosis, acanthosis and elongation of the epithelial rete ridges.
  • 67.  In the red portion of the lesion, localised loss of filiform papillae is seen with epithelial atrophy and mild subepithelial T lymphocyte infiltration.  In addition, the epithelial surface is frequently necrotic, and collections of neutrophils with formation of microabscesses are observed within the epithelium. Because these features are reminiscent of psoriasis, this is called a psoriasiform mucositis.
  • 68.  Differential diagnosis :  The histopathological appearance of mucosal lesions in psoriasis pustulosa generalisata and Reiter's syndrome cannot be distinguished from erythema migrans.  It may also be mistaken for lichen planus.
  • 70. LUPUS ERYTHEMATOSUS  Definition : Lupus erythematosus is a chronic immunologically mediated disease.  Etiology : Autoimmune. the main feature is the formation of antibodies to DNA, which may initiate immune complex reactions, in particular a vasculitis.  Clinical features : Two main forms of the disease are recognized: discoid (DLE) and systemic (SLE). Oral lesions develop in 15–25% of cases in DLE and in 30–45% of cases in SLE, usually in association with
  • 71.  Three subtypes of lupus-specific skin lesions have been described: acute, subacute, and chronic.  Acute cutaneous lupus occurs in 30 to 50% of patients and is classically represented by the butterfly rash–mask-shaped erythematous eruption involving the malar areas and bridge of the nose but typically (as opposed to dermatomyositis [DM]) sparing nasolabial folds.  Bullous lupus and localized erythematous
  • 72.  Subacute lupus – cutaneous , non indurated psoriasiform annulay polycyclic lesions that resolve without scaring , although occasionally with post inflammatory dyspigmentation  Chronic cutaneous lupus – classic discoid rash localised or generalised, hypertrophic lupus in verrucous form, mucosal lupus, lichen planus overlap
  • 73.  The oral lesions are characterized by a well- defined central atrophic red area surrounded by a sharp elevated border of irradiating whitish striae, brush border appearance.  Telangiectasia, petechiae, edema, erosions, ulcerations, and white hyperkeratotic plaques may be seen.  Buccal mucosa, gingiva, and labial mucosa are the most commonly affected intraoral sites. Isolated erythematous areas are also common, especially on the palate.
  • 74.  Differential diagnosis : Lichen planus, geographic glossitis, speckled leukoplakia, erythroplakia, cicatricial pemphigoid, syphilis.  Treatment : Steroids, Nonsteroidal anti- inflammatory drugs (nsaids) are frequently used in SLE for symptomatic relief of arthritis but are of little benefit in more severe disease.  Cyclosporine, tacrolimus, sirolimus, methotrexate, and intravenous immunoglobulins have also been used in SLE. Antimalarials, such as hydroxychloroquine, are effective in cutaneous lupus with fewer adverse effects.
  • 75.
  • 76.
  • 77. ERYTHROPLAKIA  Definition : Erythroplakia, or Queyrat erythroplasia, is a premalignant lesion that rarely occurs on the oral mucosa.  It is defined as a red patch or plaque that cannot be classified clinically or pathologically under any other condition.  Etiology : Unknown ( smoking and alcohol abuse are important risk factors )
  • 78.  Clinical features : It appears as a usually asymptomatic, fiery red, well demarcated plaque, with a smooth and velvety surface.  The red lesions may be associated with white spots or small plaques. The floor of the mouth, retromolar area, soft palate, and tongue are the most common sites of involvement.
  • 79. Homogeneous erythroplakia Erythroplakia interspersed with patches of leukoplakia Granular or speckled erythroplakia  Erythroplakia occurs more frequently between the ages of 50 and 70 years. Over 91% of erythroplakia s histologically demonstrate severe dysplasia, carcinoma in situ, or early invasive squamous-cell carcinoma at the time of diagnosis.
  • 80.  Laboratory tests : Histopathological examination.  Differential diagnosis : Erythematous candidiasis, lichen planus, early squamous-cell carcinoma, local irritation.  Treatment : cold knife Surgical excision laser surgery.
  • 82. THERMAL BURN  Definition and etiology : Thermal burns to the oral mucosa are fairly common, usually due to contact with very hot foods, liquids, or hot metal objects.  Clinical features : Clinically, the condition appears as a red, painful erythema that may undergo desquamation, leaving erosions.
  • 83.  The lesions heal spontaneously in about a week. The diagnosis is made exclusively on clinical grounds.  Differential diagnosis : Chemical burn, traumatic lesions, herpes simplex, aphthous ulcers, drug reactions.  Treatment : No treatment is required.
  • 84. DRUGS AND CHEMICAL BURN  Aspirin tablets/powder  Tooth ache drops containing creosote, guaiacol, phenol derivatives  Dental medicaments such as chromic acid, trichloroacetic acid, silver nitrate, beechwood creosote, eugenol, paraformaldehyde, ticture of iodine
  • 85. DRUGS  Erythema multiforme – antibiotics like sulfonamides, tetracyclines, amoxicillin, ampicillin. Anticonvulsants – phenytoin, barbiturates  Stevenson johnson syndrome – acetaminophen and NSAID s
  • 87. AVITAMINOSIS B12  Avitaminosis is any disease caused by chronic or long-term vitamin deficiency or caused by a defect in metabolic conversion, such as tryptophan to niacin. They are designated by the same letter as the vitamin  Avitaminosis B12 causes pernicious anemia
  • 88.  The clinical symptoms are weakness, fatigue, shortness of breath and neurologic abnormalities.  The presence of oral signs and symptoms, include glossitis, angular cheilitis, recurrent oral ulcer, oral candidiasis, diffuse erythematous mucositis and pale oral mucosa.  Management is through vitamin supplements
  • 89. VITAMIN B COMPLEX  Vitamin B1 (thiamine)  Vitamin B2 (riboflavin)  Vitamin B3 (niacin or nicotinic acid)  Vitamin B5 (Pantothenic acid)  Vitamin B6 (pyridoxine, pyridoxal, pyridoxamine)  Vitamin B7 (biotin)  Vitamin B9 (folic acid)  Vitamin B12 (various cobalamins; commonly cyanocobalamin or methylcobalamin in vitamin supplements)
  • 92.
  • 93. PURPURA  Purpura is a condition of red or purple discolored spots on the skin that do not blanch on applying pressure.  The spots are caused by bleeding underneath the skin usually secondary to vasculitis.  They measure 0.3–1 cm (3–10 mm), whereas petechiae measure less than 3 mm, and ecchymoses greater than 1 cm
  • 94.  Purpura are a common and nonspecific medical sign.  Platelet disorders (thrombocytopenic purpura)  Primary thrombocytopenic purpura  Secondary thrombocytopenic purpura  Post-transfusion purpura  Vascular disorders (nonthrombocytopenic purpura)  Microvascular injury, as seen in senile (old age) purpura, when blood vessels are more easily damaged
  • 95.  Hypertensive states  Deficient vascular support  Vasculitis, as in the case of Henoch-Schönlein purpura  Coagulation disorders - Disseminated intravascular coagulation (DIC)  Scurvy (vitamin C deficiency) - defect in collagen synthesis which results in weakened capillary walls and cells
  • 96.
  • 98. IDIOPATHIC THROMBOCYTOPENIC PURPURA  Definition Thrombocytopenic purpura is a hematological disorder characterized by a decrease in platelets in the peripheral blood.  Etiology Presumably a nonspecific viral infection, myelotoxic agents.
  • 99.  Clinical features The oral manifestations consist of red lesions in the form of petechiae, ecchymoses, or even hematomas, usually located on the palate and buccal mucosa.  Spontaneous gingival bleeding is a constant early finding.  Purpuric skin rash, epistaxis, and bleeding from the gastrointestinal and urinary tract are common.
  • 100.  Laboratory tests Peripheral platelet count, bone-marrow aspiration, bleeding and clotting times.  Differential diagnosis Aplastic anemia, leukemias, polycythemia vera, agranulocytosis, drug reactions.  Treatment Steroids, platelet transfusions, cessation of drug treatment if it is drug-related.
  • 102. TELANGECTASIA  Persistent dilatation of small, superficial blood vessels; rarely inherited  They are red seldom over 5mm in diameter and blanch readily on digital pressure, which easily differentiates them from red petechiae.  They may occur as red solitary lesions or multiple lesions.
  • 103.
  • 104.  The uncommon Osler-Weber-Rendu syndrome (hereditary haemorrhagic teleangiectasia; HHT) is inherited via an autosomal dominant trait, however, family history can be negative.  Clinically, oral and peri-oral telangiectasias are observed, as well as telangiectasias in the nose, the gastro-intestinal tract and on the palms of the hands. They may bleed which may cause chronic iron-deficiency anaemia.
  • 106. SCLERODERMA  Scleroderma is a rare autoimmune disorder of blood vessels and connective tissue, which is divided into a progressive systemic and a localised form (circumscribed scleroderma).  The disease most commonly affects adult middle-aged females. In later stages, development of a mask-like face with restricted mouth opening (microstomia), telangiectasias, smooth tongue surface and shortened lingual frenum.
  • 108. CREST SYNDROME  A relatively mild variant is characterised by subcutaneous calcification (CREST syndrome: calcinosis cutis, Raynaud's phenomenon, esophageal dysfunction, sclerodactyly and telangiectasia); frequent association with Sjögren's syndrome.
  • 110.  Differential diagnosis  Oral lesions in Osler-Weber-Rendu syndrome: scleroderma, chronic liver diseases, post- irradiation state  Oral lesions in scleroderma: Osler-Weber- Rendu syndrome, oral submucous fibrosis, secondary Sjögren's syndrome
  • 111.  Treatment and prognosis  Osler-Weber-Rendu syndrome: local haemostasis (cryo-surgery or laser), treatment of anaemia.  Scleroderma: management is difficult; enhancement of micro-circulation , corticosteroids, in some cases immunosuppressants. Prognosis is dependent on type of disease; from favourable to poor and lethal.
  • 112. ANGIOMA  Developmental vascular malformation (hamartoma) or benign vascular tumour. Two types - cavernous and capillary types.  In the oral cavity, the most common mesenchymal tumour of infancy.  Commonest localisation: tongue, lips, buccal mucosa.
  • 113.  Capillary hemangiomas are further classified into juvenile , senile , nevus flammeus  Juvenile hemangioma  Most common type of capillary hemangioma  Majority occur in head and neck region shortly after birth  Period of rapid growth then begin to regress after about a year  Fully developed hemangioma is elevated, lobulated, sharply circumscribed, and bright red  They require no treatment.
  • 115.  Senile hemangioma  Start appearing in early adulthood, and the number of lesion increases with age.  The lesions are bright red and vary in dia from 1mm to several mm s.  The larger lesions are soft and dome shaped.
  • 117.  Nevus flammeus  Also known as port wine stains, are present at birth are unilateral and located on face and neck  Sharply circumscribed and range from small red macules to large red flat patches that are blanched by pressure.  Haemangiomatous vascular malformation of the face related to maxillary division of the trigeminal nerve (port wine stain) and involvement of the leptomeninges occur in Sturge-Weber syndrome
  • 118.  Complications: epilepsy, contralateral hemiplegia (rare), mental retardation (common).
  • 119. ANGIOMAS  Angiomatous syndromes  Osler- Weber-Rendu syndrome (hereditary hemorrhagic telangiectasia)  blue rubber bleb nevus syndrome  Bannayan-Zonana  Sturge-Weber  Klippel-Trénaunay syndrome  Servelle-Martorell syndrome  von Hippel-Lindau syndrome  Maffucci’s syndrome
  • 122. ANGIOKERATOMAFABRY S DIASEASE  Angiokeratoma is a benign cutaneous lesion of capillaries, resulting in small marks of red to blue color and characterized by hyperkeratosis.  Angiokeratoma corporis diffusum refers to Fabry's disease is a rare genetic lysosomal storage disease, inherited in an X- linked manner. Fabry disease can cause a wide range of systemic symptoms. It is a form of sphingolipidosis, as it involves dysfunctional metabolism of sphingolipids.
  • 123.  Clinical features – dermatological manifeatations – Angiokeratomas occur commonly on the thighs, lower abdomen, and groin)  Anhidrosis (lack of sweating) is a common symptom, and less commonly hyperhidrosis (excessive sweating).  Ocular involvement may be present showing cornea verticillata (also known as vortex keratopathy), i.e. clouding of the corneas. This clouding does not affect vision.
  • 124. HISTOPATHOLOGY  Angiokeratomas characteristically have large dilated blood vessels in the superficial dermis and hyperkeratosis (overlyin g the dilated vessels).
  • 125.
  • 127. SQUAMOUS CARCINOMA  The early stage of squamous-cell carcinoma may present as an asymptomatic, atypical red patch.  The clinical features are identical to erythroplakia, erythematous candidiasis, or contact reactions to dental materials.  In these cases, a biopsy should be taken to allow a conclusive diagnosis.
  • 128.
  • 129.
  • 130.
  • 131. KAPOSIS SARCOMA  Malignant neoplasm composed of spindle cells and vascular elements  Occurs in homosexual men affected with AIDS commonly  Classic , Endemic and epidemic types  Classic or sporadic type – commonly occurs in older persons of jewish origin, involves the skin of lower extremities  Oral mucosal involvement is rare in this
  • 132.  Endemic form – occurs in native black population  Epidemic form affects those with HIV and other immunological disorder  Lesions widely distributed over the skin  Mucosa and lymph nodes are involved and response to treatment is poor
  • 133.  KS can involve any oral site but most frequently involves the attached mucosa of the palate, gingiva, and dorsum of the tongue.  Lesions begin as blue purple or red purple flat discolorations that can progress to tissue masses that may ulcerate.  The lesions do not blanch with pressure. Initial lesions are asymptomatic but can cause discomfort and interfere with speech, denture use, and eating when lesions progress.
  • 134.
  • 135.  The differential diagnosis includes ecchymosis, vascular lesions, and salivary gland tumors.  Definitive diagnosis requires biopsy. Because KS is a multicentric neoplastic disease, multiple sites of involvement can occur, including skin, lymph nodes, gastrointestinal tract, and other organ systems.
  • 136. TREATMENT  Surgical excision, electrocautery and radiation therapy.  Patients with disseminated disease may be treated with immunomodulators and single agent or combination chemotherapy.
  • 137.
  • 138.
  • 139. WEGENER S GRANULOMATOSIS  Granulomatosis with polyangiitis (GPA), formerly referred to as Wegener's granulomatosis (WG), is a systemic disorder that involves both granulomatosis and polyangiitis.  It is a form of vasculitis (inflammation of blood vessels) that affects small- and medium-size vessels in many organs  Oral cavity: strawberry gingivitis, underlying bone destruction with loosening of teeth, non- specific ulcerations throughout oral mucosa
  • 140.
  • 141. MIDLINE LETHAL GRANULOMA  Lethal midline granuloma is a condition affecting the nose and palate.  Macroscopically the lesions usually look like necrotic granulomas and are characterized by ulceration and destruction of the nose and paranasal sinuses with erosion of soft tissues, bone and cartilage of the region.
  • 142.  The patients show an aggressive and lethal course with rapid destruction of the nose and face (midline), therefore the term “lethal midline granuloma”.  This disease occurs around the fourth decade and occurs commonly in males.
  • 143.  The major symptoms are nasal stuffiness with or without nasal discharge.  Oral or nasal ulcer with conjunctivitis may also occur. Perforation of the nasal septum with mutilation of the surrounding tissues eventually occurs.  Morphologically it is characterized by extensive ulceration of mucosal sites with a lymphomatous infiltrate that is diffuse, but has an angiocentric and angiodestructive growth pattern.
  • 144.
  • 146. DENTURE STOMATITIS  Definition : Denture stomatitis, or denture sore mouth, is a frequent condition in patients who wear dentures continuously for extended times.  Etiology : Mechanical irritation from dentures, Candida albicans, or a tissue response to microorganisms living beneath the dentures.  Also caused by bacteria such as streptococcus, veillonella, lactobacillus, prevotella and actinomyces.
  • 147.  Clinical features : The condition is characterized by diffuse erythema, edema, and sometimes petechiae and white spots that represent accumulations of candidal hyphae, almost always located in the denture bearing area of the maxilla.  The condition is usually asymptomatic. The diagnosis is based on clinical criteria.  Type I – localised to minor erythematous areas caused by trauma from denture
  • 148.  Type II – affects major part of denture covered mucosa  Type III – granular mucosa in the central part of the palate  Differential diagnosis : Allergic contact stomatitis due to acrylic.  Treatment : Improvement of denture fit, proper oral hygiene, and topical antimycotics.
  • 150. MEDIAN RHOMBOID GLOSSITIS  Definition : Median rhomboid glossitis is a rare condition that occurs exclusively on the dorsum of the tongue.  Etiology : Presumably developmental, Candida albicans , bacteria may also be involved.  Clinical features : It presents as a well- demarcated erythematous rhomboid area,
  • 151.  along the midline of the dorsum of the tongue, immediately anterior to the circumvallate papillae.  The surface of the lesion may be smooth or lobulated. Atrophy of filiform papillae.  Differential diagnosis : Candidiasis, lymphangioma, geographic tongue, syphilis, hemangioma.  Treatment : No treatment is required.
  • 152. KISSING LESIONS  A concurrent erythematous lesion may be observed in the palatal mucosa and it is called kissing lesion.  Management is restricted to a reduction in predisposing factors.
  • 153. KISSING LESION ON THE PALATE
  • 155. RADIATION MUCOSITIS  Definition and etiology : Oral radiation mucositis is a side effect of radiation treatment of head and neck tumors.  Clinical features : The oral lesions are classified as early and late. Early reactions may begin at the end of the first week of radiotherapy, and consist of erythema and edema of the oral mucosa.
  • 156.  Soon after, erosions or ulcers may develop, covered by a whitish-yellow exudate.  Xerostomia, loss of taste, and burning and pain during mastication, swallowing, and speech are common. The diagnosis is made clinically.
  • 157.  Differential diagnosis : Mucositis due to chemotherapy, graft-versushost disease, erythema multiforme, herpetic stomatitis, lichen planus.  Treatment : Supportive treatment. Cessation of the radiation treatment, B-complex vitamins, and sometimes low doses of steroids are indicated.
  • 159. POLYCYTHEMIA  Also called erythremia is chronic and sustained elevation in the number of erythrocytes and level of hemoglobin.  Primary  secondary
  • 160.  Primary – polycythemia vera is a neoplastic condition of erythropoietic sysyem  Secondary – is a sustained elevation of erythrocytes and hemoglobin usually resulting from bone marrow stimulation caused by living at high altitude or chronic pulmonary disease such as emphysema
  • 161.  The entire oral mucosa of patients with polycythemia has a deep red or purple color.  Soft palate and gingiva are prone to easy bleeding and petechial hemorrhages may be seen on the palate and labial mucosa  Infarcts may occur in the smaller blood vessel leading to ulcers
  • 162.
  • 163. DIAGNOSIS  Increase in erythrocytes  Hemoglobin concentration  hematocrit
  • 164. PLASMA CELL GINGIVITIS  Definition : Plasma-cell gingivitis is a rare and unique gingival disorder, characterized histopathologically by a dense chronic inflammatory infiltration of the lamina propria, mainly of plasma cells.  Etiology : Unknown. Reactions to local allergens, chronic infections, and plasma-cell dyscrasias have been considered as possible causes.
  • 165.  Clinical features : Clinically, both free and attached gingiva are bright red and edematous, with a loss of normal stippling. The gingivitis may be localized or widespread, and is frequently accompanied by a burning sensation.  Rarely, similar lesions may be seen on the tongue and lips.  Ulcers , epithelial sloughing and desquamation may be present.  Patient may complain of pain, sensitivity and bleeding of gingiva during brushing.
  • 166.  Laboratory tests : patch testing to identify the allergen, Histopathological and histochemical examination, immunofluorescence.  Histopathology : parakeratosis , epithelial hyperplasia , dense infiltrate of plasma cells in the lamina propria , dilated blood capillaries.  Differential diagnosis : Desquamative gingivitis, erosive lichen planus, vesiculobullous disorders.
  • 167.  Pubertal or pregnancy induced gingivitis, plaque associated gingivitis.  Rapid onset - PCS.  Treatment : Remove the allergen if possible. Pain control, Topical or systemic steroids.  Gingivectomies to recontour lesions that are long standing and fibrotic.
  • 169.
  • 172. ERYTHEMA MULTIFORME  EM is an acute, self-limited, inflammatory mucocutaneous disease that manifests on the skin and often oral mucosa, although other mucosal surfaces, such as the genitalia, may also be involved.
  • 173.  EM is classified as E M minor if there is less than 10% of skin involvement and there is minimal to no mucous membrane involvement, whereas EM major has more extensive but still characteristic skin involvement, with the oral mucosa and other mucous membranes affected.  Historically, fulminant forms of EM were labeled Stevens- Johnson syndrome (SJS) and toxic epidermal necrolysis [TEN (Lyell disease)].
  • 174. ETIOLOGY  EM is a hypersensitivity reaction, and the most common inciting factors are infection, particularly with HSV, or drug reactions to NSAIDS or anticonvulsants.  Other viral, bacterial, fungal, and protozoal infections and medications may also play a role.
  • 175. CLINICAL FEATURES  EM generally affects those between ages 20 and 40 years, with 20% occurring in children.  There is often a prodrome of fever, malaise, headache, sore throat, rhinorrhea, and cough.  Skin lesions begin as red macules that become papular, starting primarily in the hands and moving centripetally toward the trunk in a symmetric distribution. The most common sites of involvement are the upper extremities, face, and neck.
  • 176.  The skin lesions may take several forms— hence the term multiforme - irregular bullae, erosions, or ulcers surrounded by extensive areas of inflammation, Severe crusting and bleeding of the lips are common.  The classic skin lesion consists of a central blister or necrosis with concentric rings of variable color around it called typical “target” or “iris” lesion that is pathognomonic of EM; variants are called “atypical target” lesions .
  • 177.
  • 178. ORAL MANIFESTATIONS  mild erythema and erosion to painful ulcerations.  When severe, ulcers may be large and confluent, causing difficulty in eating, drinking, and swallowing, and patients with severe EM may drool blood-tinged saliva.
  • 179.
  • 180.  Differential diagnosis : Primary HSV gingivostomatitis, Autoimmune vesiculobullous disease such as pemphigus and pemphigoid, recurrent aphthous ulcers.  Management : systemic or topical analgesics, corticosteroids, antiviral medication, azathioprine and dapsone , antimalarials prevents recurrence.
  • 181. REFERENCES  Peripheral giant cell granuloma Padam Narayan Tandon, S. K. Gupta,1 Durga Shanker Gupta, Sunit Kumar Jurel,2 and Abhishek Saraswat  Oral Manifestations of Vitamin B12 Deficiency: A Case Report Hélder Antônio Rebelo Pontes, DDS, MSc, PhD; Nicolau Conte Neto, DDS; Karen Bechara Ferreira, DDS; Felipe Paiva Fonseca; Gizelle Monteiro Vallinoto; Flávia Sirotheau Corrêa Pontes, DDS, MSc, PhD; Décio dos Santos Pinto Jr, DDS, MSc, PhD
  • 182.  Text book of Burket s oral medicine  Text book of Differential Diagnosis of oral and maxillofacial lesions by Norman K Wood and Paul W Goaz  Shafer s text book of oral pathology