Red Blue lesions

Done By :
Weam Mahmoud Faroun
NEOPLASMS
 INTRAVASCULAR LESIONS
• CONGENITAL VASCULAR ANOMALIES
• Congenital Hemangiomas and Congenital Vascular
Malformations

• MalformationsEncephalotrigeminal Angiomatosis
(Sturge-Weber Syndrome)

• Hereditary Hemorrhagic Telangiectasia (Rendu-

Osler-Weber Syndrome)
Etiology
• appear at or around the time of birth
• more common in females.
• Unfortunately, difficulty in classifying lesions because
of overlapping clinical and histological features.
• congenital hemangiomas subdivided into two
microscopic types—capillary and cavernous—
essentially reflecting differences in vessel diameter.
• Vascular malformations may exhibit similar features
but may also show vascular channels that represent
arteries and veins.
Clinical features
Clinical Features
• Congenital hemangioma also known as
strawberry nevus, usually appears around the
time of birth, but may not be apparent until
early childhood .This lesion may exhibit a rapid
growth phase that is follow several years later
by an involution phase.
• In contrast, congenital vascular malformations
are generally persistent lesions that grow with
the individual.
• Both types of lesions may range in color from red
to blue, depending on the degree of congestion
and their depth in tissue.
• When they are compressed, blanching occurs as
blood is pressed peripherally from the central
vascular spaces.
• This simple clinical test (diascopy) can be used to
separate these lesion from hemorrhagic lesions in
soft tissue (ecchymoses), where the blood is
extravascular and cannot be displaced by
pressure.
• Congenital hemangiomas and congenital
vascular malformations may be fat, nodular, or
bosselated.
• Lesions are most commonly found on the lips,
tongue, and buccal mucosa.
• Lesions that affect bone are probably
congenital vascular malformations rather than
congenital hemangiomas.
• Vascular malformations are also a component of
the rare termed blue rubber bleb nevus
syndrome (Bean’s syndrome),in which multiple
small and large cavernous hemangiomas are
present on the skin and throughout the
gastrointestinal tract, including the mouth.
• The condition is usually diagnosed in childhood or
young adulthood. Recognition of this syndrome is
significant because many of those afflicted may
suffer overt life-threatening gastrointestinal
bleeding or occult blood loss with severe anemia
and iron deficiency.
Diagnosis
 Diagnosis.
• the diagnosis of lesions by clinical examination.
• When they affect the mandible or the maxilla, a radiolucent
lesion with a honeycomb pattern and distinct margins is
expected.
• Differentiation between congenital hemangiomas and
congenital vascular malformations can be difficult and
occasionally impossible.
• When affecting a segmental portion of the face or oral
cavity, facial hemangiomas may be associated with several
syndromes, which may include the eye, heart, and
posterior cranial fossa (PHACE syndrome).
• A complete history, a clinical examination, and angiography
or angiographic magnetic resonance imaging should be
definitive in lesion identification and characterization.
 Treatment
• Spontaneous involution during early childhood
is likely for congenital hemangiomas. If these
lesions persist into the later years of childhood,
involution is improbable and definitive treatment
may be required.
• Congenital vascular malformations generally do
not involute, and they require intervention if
eradication is the goal.
• Laser therapy is another accepted form of
primary treatment of selected vascular lesions.
• Because the margins of these lesions are often ill
defiend, total elimination may not be practical or
possible.
• a neurocutaneous syndrome that includes vascular
malformations with characteristic distribution.
• In this syndrome, venous malformations involve the
leptomeninges of the cerebral cortex, usually with
similar vascular malformations of the face
• The associated facial lesion, also known as portwine
stain or nevus fammeus, involves the skin innervated by
one or more branches of the trigeminal nerve.
• The vascular defect may extend intraorally to involve the
buccal mucosa and the gingiva
• Ocular lesions may appear.
• Neurologic effects may include mental retardation,
hemiparesis, and seizure disorders.
• Patients may be taking phenytoin (Dilantin) or similar
drugs for control of the latter problem, with possible
secondary development of drug-induced generalized
gingival hyperplasia in relation to phenytoin.
• Calcification of the intracranial vascular lesion may
provide radiologic evidence of the process in the
leptomeninges.
• A differential diagnosis would include Parkes-Weber
syndrome and angioosteohypertrophy (Klippel-
Trenaunay) syndrome, the latter characterized by
vascular malformations of the face (port-wine stains),
varices, and hypertrophy of bone.
• The bony abnormality usually affects long bones but
may also involve the mandible or maxilla, resulting in
asymmetry, malocclusion, and an altered eruption
pattern.
• is a rare condition, affecting 1 in 5000 to 8000
people, that is transmitted in an autosomal-
dominant manner.
• Most cases are caused by mutations in two genes
These genes are members of the transforming
growth factor (TGF)-β signaling pathway and are
implicated in vascular development and repair.
• features : abnormal and fragile vascular dilations
of terminal vessels in skin and mucous
membranes, as well as arteriovenous
malformations of internal organs, particularly
lungs, brain, and liver
• Telangiectatic vessels in this condition appear clinically
as red macules or papules, typically on the face, chest,
and oral mucosa.
• Lesions appear early in life, persist throughout
adulthood, and often increase in number with aging.
• Intranasal telangiectasias are responsible for epistaxis,
the most common presenting sign of hereditary
hemorrhagic telangiectasia. Bleeding from oral lesions
is a common occurrence in affected patients.
Occasionally, control of bleeding may be a difficult
problem.
• Chronic low-level bleeding may also result in iron
deficiency anemia.
• Diagnosis is based on a history of spontaneous
epistaxis, the presence of telangiectasias,
arteriovenous malformations of internal organs,
and family history.
• Another condition that might be considered in a
differential diagnosis is CREST syndrome. This
includes calcinosis cutis, Raynaud’s phenomenon,
esophageal dysfunction, sclerodactyly, and
telangiectasia.
• Clinical management includes follow-up
examination and the use of antifibrinolytic drugs
for those with frequent epistaxis.
Varix and Other Acquired
Vascular Malformations

Pyogenic Granuloma

Peripheral Giant Cell

Granuloma
• A venous varix, or varicosity, is a type of acquired vascular
malformation that represents focal dilation of a single
vein.
• It is a relatively trivial but common vascular malformation
when it appears in the oral mucosa and lips .
• *Varices involving the ventral aspect of the tongue are
common developmental abnormalities.
• * Varices are also common on the lower lip in older
adults, representing vessel wall weakness caused by
chronic sun exposure with subsequent dilation.
• Varices typically are blue and blanch with compression.
• No treatment is required for a venous varix unless it is
frequently traumatized or is cosmetically objectionable.
 Etiology.
• Pyogenic granuloma represents an increased
connective tissue proliferation to a known
stimulus or injury.
• It appears as a red mass because it is composed
predominantly of hyperplastic granulation tissue
in which capillaries are very prominent.
• The term pyogenic granuloma is a misnomer in
that it is not pus producing, and it does not
represent granulomatous infammation
 Clinical Features.

• occur mostly in the second decade of life

• are most commonly seen on the attached gingiva
(75%), where they presumably are caused by the
presence of calculus or foreign material within
the gingival crevice
• The tongue, lower lip, and buccal mucosa are the
next most common sites.
• Pyogenic granulomas are typically red and
smooth or lobulated with hemorrhagic and
compressible features.
• They characteristically become ulcerated
because of secondary trauma.
• The ulcerated lesions may then become
covered by a yellow, fibirnous membrane.
• may range in size from a few millimeters to
several centimeters.
• Older lesions become more pink and
collagenized.
• seen at any age
• more commonly in females than in males
• seen up to 5% of pregnancies.
 Differential Diagnosis
• Clinically, this lesion is similar to peripheral giant cell
granuloma, which also presents as a red gingival mass.
• A peripheral odontogenic or ossifying fibroma may be
another consideration, although these tend to be much
lighter in color.
• Less commonly, other conditions that may be
considered include Kaposi’s sarcoma, bacillary
angiomatosis, and non-Hodgkin’s lymphoma.
• Rarely, metastatic cancer may present as a red gingival
mass.
• Biopsy findings are definitive in establishing the
diagnosis.
 Treatment
• Pyogenic granulomas should be surgically excised;
removal should include the connective tissue from
which the lesion arises, as well as local etiologic factors
(plaque, calculus, foreign material, source of trauma).
• Recurrence is occasional and is believed to result from
incomplete excision, failure to remove etiologic factors,
or reinjury of the area.
• The end of pregnancy often brings considerable
shrinkage of pregnancy-associated pyogenic
granulomas, but residual lesions may need to be
excised.
 Etiology
• relatively uncommon
• unusual hyperplastic connective tissue response
to injury of gingival tissues.
• It is one of the “reactive hyperplasias” commonly
seen in oral mucous membranes, representing an
exuberant reparative process in association with
local trauma or irritation.
• The feature that sets this lesion apart from the
others is the appearance of multinucleated giant
cells, but the reason for their presence remains
unknown.
 Clinical Features.
• seen exclusively in gingiva, usually between the first
permanent molars and the incisors .
• arise from periodontal ligament or periosteum, and they
cause, on occasion, resorption of alveolar bone.
• When this process occurs on the edentulous ridge, a
superficial, cup-shaped radiolucency may be seen.
• Peripheral giant cell granulomas typically appear as red to
blue, broad-based masses.
• Secondary ulceration caused by trauma may result in the
formation of a fibrin clot over the ulcer.
• most are about 1 cm in diameter
• may occur at any age
• more commonly in females than in males.
 Differential Diagnosis
• Generally, this lesion is clinically indistinguishable
from a pyogenic granuloma.
• Although a peripheral giant cell granuloma is
more likely to cause bone resorption than is a
pyogenic granuloma, the differences are
otherwise minimal.
• A biopsy provides definitive diagnostic results.
• Microscopically, a peripheral giant cell granuloma
is identical to its central or intraosseous
counterpart, the central giant cell granuloma.
 Treatment.
• Surgical excision is the preferred treatment for
peripheral giant cell granulomas.
• Removal of local factors or irritants is also
required.
• Recurrences, which are seen occasionally, are
believed to be related to lack of inclusion of
periosteum or periodontal ligament in the
excised specimen.
 NEOPLASMS
Erythroplakia

Kaposi’s Sarcoma
 Etiology
• Erythroplakia is a clinical term that refers to a red
patch on oral mucous membranes.
• It does not indicate a particular microscopic diagnosis,
although after a biopsy most cases are found to be
severe dysplasia or carcinoma.
• The causes of this lesion are believed to be similar to
those responsible for oral cancer.
• Therefore tobacco use probably has a significant role in
the induction of many of these lesions, as does heavy
alcohol consumption. Nutritional deficits and other
factors may have modifying roles.
 Clinical Features
• Erythroplakia is seen much less commonly than
its white lesion counterpart, leukoplakia.
• A strong association with tobacco consumption
and use of alcohol has been noted. In comparison
with leukoplakia, it should, however, be viewed
as a more serious lesion because of the
significantly higher percentage of malignancies
associated with it
• The lesion appears as a red patch with well-
defined margins
• Common sites of involvement include the floor of
the mouth, the tongue, retromolar mucosa, and
the soft palate.
• Individuals between 50 and 70 years of age are
usually affected, and no gender predilection is
apparent.
• Focal white areas representing keratosis may be
seen in some lesions (erythroleukoplakia).
Erythroplakia is usually supple to the touch
unless the lesion is invasive, in which case
induration may be noted.
 Histopathology.
• Approximately 40% of erythroplakias show severe
dysplastic change; about 50% are squamous cell carcinoma
and 9% mild or moderate dysplasia.
• A relative reduction in keratin production and a relative
increase in vascularity account for the clinical color of these
lesions.
• A histologic variant of carcinoma in situ exhibits changes
analogous to the skin lesion called Bowen’s disease.
• Microscopic features that separate this bowenoid change
from the usual carcinoma in situ include marked disordered
growth, multinucleated keratinocytes, large
hyperchromatic keratinocyte nuclei, and atypical individual
cell keratinization.
 Differential Diagnosis
• should include Kaposi’s sarcoma, ecchymosis,
contact allergic reaction, vascular
malformation, and psoriasis.
• The clinical history and examination should
distinguish most of these lesions.
• A biopsy provides a definitive answer
 Treatment
• The treatment of choice for erythroplakia is surgical
excision.
• Generally, it is more important to excise widely than to
excise deeply in dysplastic and in situ lesions because
of their superficial nature and the fact that dysplastic
cells usually extend beyond the clinically evident
lesion.
• However, because epithelial changes may extend along
the salivary gland excretory ducts in the area, the deep
surgical margin should not be too shallow
• Several histological sections may be necessary to
adequately assess the involvement of salivary ducts
• It is generally accepted that severely dysplastic
and in situ erosions eventually become
invasive.
• The time required for his event can range from
months to years.
• Follow-up examinations are critical for
patients with these lesions because of the
potential field effect and corresponding
genetic and molecular alterations caused by
etiologic agents.
 Etiology
• Kaposi’s sarcoma is a proliferation of endothelial cell
origin, although dermal/submucosal dendrocytes,
macophages, lymphocytes, and probably mast cells
may have a role in the genesis of these lesions.
• A relatively recently disovered herpesvirus known as
human herpesvirus 8 (HHV8), or Kaposi’s sarcoma
herpesvirus (KSHV), has been identified in all forms of
Kaposi’s sarcoma lesions, as well as in acquired
immunodeficiency syndrome (AIDS)-associated body
cavity lymphomas and in multicentric Castleman’s
disease.
• This virus is believed to have a significant role in the
induction and/or maintenance of Kaposi’s sarcoma
through perturbation of focally released cytokines and
growth factors via virally encoded microRNAs.
 Clinical Features
• Three different clinical patterns of Kaposi’s
sarcoma have been described
• In this classic form, it appears as multifocal
reddish-brown nodules primarily in the skin of
the lower extremities, although any organ may be
affected
• Oral lesions are rare in this type.
• This classic form has a rather long indolent course
and only a fair prognosis.
• The most commonly affected organ is the skin.
• Oral lesions are rarely seen.
• The clinical course is prolonged, and the overall
prognosis is only fair.
• The third pattern of Kaposi’s sarcoma has been seen in
patients with immunodeficiency states, including
patients with organ transplants and especially AIDS
• This type differs from the other two forms in several
ways.
• Skin lesions are not limited to the extremities, and they
may be multifocal.
• Oral mucosal and regional lymph node lesions are
relatively common. Visceral organs may also be
involved, and a younger age group is afected.
• The clinical course is relatively rapid and aggressive,
and the prognosis is correspondingly poor.
• Kaposi’s sarcoma, once occurring in about one third of
patients with AIDS, is now seen with considerably less
frequency—a shift that appears to be related to
suppression of human immunodefciency virus (HIV)
replication by antiretroviral drug therapy and concurrent
improvement in CD4 lymphocyte levels, particularly with
the use of highly active antiretroviral therapy (HAART).
• About half of AIDS- affected patients with cutaneous
Kaposi’s sarcoma develop oral lesions.
• Of significance is that oral lesions may be the initial site or
the only site of involvement.
• Kaposi’s sarcoma has been described in most oral regions,
although the palate, gingiva, and tongue seem to be the
most commonly affected sites
• Clinical presentation of oral Kaposi’s sarcoma
ranges from early, rather trivial-appearing, fat
lesions to late, nodular, exophytic lesions.
Lesions may be single or multifocal.
• The color is usually red to blue.
• AIDS-affected patients with oral Kaposi’s
sarcoma may have other oral problems
concomitantly, such as candidiasis, hairy
leukoplakia, advancing periodontal disease,
and xerostomia.
 Differential Diagnosis
Clinical considerations include hemangioma, erythroplakia,
melanoma, and pyogenic granuloma.
• Another remarkable look-alike, known as bacillary
angiomatosis, mimics Kaposi’s sarcoma both clinically and
microscopically.
• The causative organism is Bartonella henselae or Bartonella
quintana.
• Cats are reservoirs for this organism, and feas may be
vectors.
• Microscopically, neutrophils and bacterial colonies are
seen.
• This condition is cured with erythromycin or tetracycline
therapy. Bacillary angiomatosis is uncommon in the skin
and is very rare in oral mucous membranes.
 Treatment
• Various forms of treatment have been used for Kaposi’s
sarcoma, but none has been uniformly successful.
• Surgery has been useful on localized lesions, and low-dose
radiation and intralesional chemotherapy have been used.
• For larger and multifocal lesions, systemic
chemotherapeutic regimens are being used.
• Improvement in the underlying immunosuppression may
help to reduce the size and number of the lesions.
• In cases of Kaposi’s sarcoma associated with organ
transplant–related immunosuppression and HIV disease,
resolution has been achieved by alteration of the
immunosuppression regimen and antiretroviral therapy.
Thank You