RED-BLUE LESIONS (OPATH2-MIDTERMS)

3 categories of red-blue lesions

• Intravascular, focal

• Intravascular, diffuse

• Extravascular

2 lesions under hemangioma

• congenital hemangioma

• vascular malformations

hemangioma

Encompasses a variety of vascular neoplasms, hamartomas, and malformations that appear predominantly at or around birth

hypovolemic shock

type of shock involved in hemangioma

congenital hemangioma

Used to identify benign congenital neoplasms of proliferating endothelial cells (capillary & cavernous)

Vascular Malformations

Include lesions resulting from abnormal vessels morphogenesis (affecting arteries and veins)

hemangioma

clinical features:

• Generally both lesions may range in color from red to blue depending upon the congestion and depth in tissue

• When compressed, blanching occurs (Clinical test to separate from hemorrhagic lesion)

• Lesion may be flat, nodular or bosselated (dangerous to tongue)

hemangioma

clinical features:

• Lesions are commonly found in the lips, buccal mucosa, and tongue

• Intranasal lesions are responsible for epistaxis, the most common presenting sign of Rendu-Osler-Weber syndrome

• Bleeding from oral lesions is also a frequent occurrence

• Venous varix or varicosity

• Abnormal vascular dilatation

• Varices in the ventral side of the tongue are common developmental abnormalities

• Also common on the lower lip in older adults

strawberry nevus

another term for congenital hemangioma

congenital hemangioma

• Usually presents around the time of birth or may not be apparent until childhood 

• Results from increased number of capillaries

• Exhibit a rapid growth phase

• Involution at later phase

• rarely affect bone

vascular malformations

• Due to abnormality of vessel morphogenesis

• Results from dilatation of arteries, veins or capillaries

• Generally persistent lesions that grow with the individual

• Do not involute

• May produce bruit or thrill

• Frequently affecting bone

Portwine Stain or Nevus Flammeus

• Involves the skin innervated by one or more branches of the trigeminal nerve

• May occur as isolated lesions of the skin without the other stigmata of Sturge-Weber syndrome

Angioosteohypertrophy Syndrome

• Characterized by vascular malformations of the face, varices and hypertrophy of the bone

• May involve mandible or maxilla resulting in asymmetry, malocclusion and altered eruption pattern

Angioosteohypertrophy Syndrome

Has one larger area because of vascular malformation; it gets bigger

Hereditary hemorrhagic telangiectasia

another term for Rendu-Osler-Weber Syndrome

Hereditary hemorrhagic telangiectasia

• A rare condition featuring abnormal vascular dilatations of terminal vessels in skin, mucosa and occasionally viscera

• Appear as red macules or papules 

• Typically affecting the face, chest and oral mucosa

• Lesions appear early in life and persist throughout adulthood

Encephalotrigeminal angiomatosis

another term for Sturge-Weber Syndrome

Sturge-Weber Syndrome

• Condition that includes vascular malformations

• Venous malformations involve the leptomeninges of the cerebral cortex, usually similar vascular malformations of the face

• May extend intraorally  to involve the buccal mucosa and gingiva

• Ocular lesions may also appear

• Neurologic defects include mental retardation, hemiparesis and seizure disorders 

• Calcification of the intracranial vascular lesion may provide radiologic evidence of the process in the leptomeninges

• Port-wine stain/nevus flames = facial lesion

Sturge-Weber Syndrome

diagnosis:

• Complete history taking, clinical examination and angiography should be definitive

Sturge- Weber Syndrome

treatment:

• Center around a careful surgical approach

• Selective arteriole embolization and sclerosant therapy

• Laser therapy is a valid form of primary treatment of selected vascular lesions

Hemangioma (2nd) ; Vascular Malformation (3rd)

Description	Abnormal endothelial cell proliferation	Abnormal blood vessel development
Elements	Results in increased number of capillaries	A mix of arteries, veins,, and capillaries (includes arteriovernous stunt)
Growth	Rapid congenital growth	Grows with patient
Boundaries	Often circumscribed; rarely affects bone	Poorly circumscribed; may affect bone
Thrill and bruit	No associated thrill and bruit	May produce thrill and bruit
Involution	Usually undergoes spontaneous involution	Does not involute
Resection	Persistent lesions resectable	Difficult to resect; surgical hemorrhage
Recurrence	Uncommon	Common

5 Developmental lesions

• hemangioma (congenital hemangioma & vascular malformation)

• portwine stain or nevus flammeus

• Angioosteohypertrophy syndrome

• Rendu-Osler-Weber Syndrome

• Sturge-Weber Syndrome

4 Reactive lesions

• pyogenic granuloma

• peripheral giant cell granuloma

• gingival reactive hyperplasias

• median rhomboid glossitis

Pyogenic Granuloma

• This lesion represents an overexuberant connective tissue reaction to a known stimulus or injury

• Appears as a red mass because it is composed predominantly of hyperplastic granulation tissue in which the capillaries are very prominent

Pyogenic Granuloma

clinical features:

• Commonly seen on the gingiva

• Caused by calculus or foreign material within the gingival crevice

• hormonal changes of puberty and pregnancy

• Typically red by may become ulcerted because of secondary trauma

• More frequently seen in females

• May appear at any age

• May range in size

• Multiple gingival lesion or generalized gingival hyperplasia

Pyogenic Granuloma

histopathology:

• Lobular masses of hyperplastic granulation tissue

• Variable number of chronic inflammatory cells may be seen

Pyogenic Granuloma

differential dx:

• Peripheral giant cell granuloma which occur as a red gingival mass

• Peripheral fibroma, but it is lighter in color

• Biopsy will give definitive diagnosis

Pyogenic Granuloma

treatment:

• Surgically excised

• Should include the removal of the connective tissue

• Removal of the etiologic factors

• Recurrence is occasionally seen due to the incomplete removal of the etiologic factor

Peripheral Giant Cell Granuloma

• Represents a relatively uncommon and unusual hyperplastic connective tissue response to injury of gingival tissues

• One other reactive hyperplasia commonly seen in oral mucosa

• Appearance of multinucleated giant cells

• Seen exclusively in gingiva along the 1st permanent molars and incisors

• Arises from periodontal ligament or periosteum and cause resorption of the alveolar bone (occasional)

Peripheral Giant Cell Granuloma

• When occur in edentulous ridge - A superficial cup-shaped radiolucency may be seen

• Typically present as red to blue broad-based masses about 1 cm in size

• Secondary ulceration due to trauma may give the lesion a focal yellow zone ( fibrin clot formation)

• May occur at any age

• More frequently seen in females

Peripheral Giant Cell Granuloma

histopathology:

• Scattered throughout the lobulated granulation tissue mass are abundant multinucleated giant cells

• Presence of chronic inflammatory cells

• More likely to cause bone resorption than pyogenic granuloma

• Biopsy will give a definitive diagnosis

Peripheral Giant Cell Granuloma

treatment:

• Surgical excision is the preferred treatment

• Removal of local factors or irritants is also required

• Recurrence is uncommon

Pyogenic Granuloma (2nd); Peripheral Giant Cell Granuloma (3rd)

Etiology	- Initiated by trauma or irritation - Modified by hormones, drugs	- Probably trauma  or irritation - Not related to hormones or drugs
Location	Predominantly gingiva, but any traumatized soft tissue	Exclusively gingival  Use anterior to first molars
Histopathology	- Hyperplasia granulation tissue - Misnomer – Neither pus producing nor granulomatous	Grows with patient
Treatment	Often circumscribed; rarely affects bone	Poorly circumscribed; may affect bone
Recurrence	Uncommon	Common

Median Rhomboid Glossitis

clinical features:

• Believed to be related to a chronic infection caused by Candida albicans

• Once thought to be a congenital abnormality related to the persistence of an embryonic midline tongue structure known as the tuberculum impar

• A red elevated rhomboid or oval lesion in the dorsal midline of the tongue, just anterior to the circumvallate papillae

  • Anything posterior to circumvallate papillae is not considered as median rhomboid glossitis anymore

• Lesion may occasionally be mildly painful, although most are asymptomatic

Median Rhomboid Glossitis

Histopathology:

• Microscopically, epithelial hyperplasia is evident in the form of bulbous rete ridges

• Candida albicans hyphae can be found in the upper levels of the epithelium

Median Rhomboid Glossitis

differential dx:

• Diagnosis is evident from the clinical appearance

Median Rhomboid Glossitis

treatment:

• No treatment is necessary

• If the lesion is painful, symptomatic treatment or use of clotrimazole troches may be necessary

• If suspect of malignancy, biopsy should be done

• Generally, no malignant potential

2 Neoplasms

• erythroplakia

• kaposi sarcoma

Erythroplakia

red patch on oral mucosa

Erythroplakia

• After biopsy, most  erythroplakia will be found to be severe dysplasia or carcinoma

• Unknown cause

• Etiologic factors are similar to those responsible for oral cancer

  • Smoking, reverse smoking, betel nut chewing, drugs

• Tobacco, alcohol, nutritional defects, & chronic irritation play contributory factor

• Seen less frequently than its leukoplakia counterpart

• More serious lesion than leukoplakia because of the significantly higher percentage of malignancies associated with it

Erythroplakia

clinical features:

• Appears as red patch with fairly well defined margins

• May be seen in any oral region

• Most commonly found in the floor of the mouth, next is the retromolar area

• Affecting 50-70 years of age

• No gender predilection

• Focal white areas representing keratosis may also be seen in some lesions

• Usually supple to touch

• Some induration may be noted in invasive lesions

Erythroplakia

histopathology:

• 90% show at least severe dysplastic change

  • 50% are invasive squamous cell carcinoma

  • 40% are severe dysplasias or carcinoma in situ

• Remainder are mild to moderate dysplasias

• Bowen’s disease - A histologic subtype of carcinoma in situ

• Seen as red (or white) patch in the oral mucosa

When occur in the glans penis – Erythroplasia of Queyrat

Bowen’s disease

A histologic subtype of carcinoma in situ

Erythroplasia of Queyrat

erythroplakia that occurs in the glans penis

Erythroplakia

differential dx:

• Atrophic candidiasis

• Macular form of Kaposi’s sarcoma

• Ecchymosis patch

• Contact allergic reaction

• Vascular malformation

• Psoriasis

• Biopsy provides definitive answer

Erythroplakia

treatment:

• Treatment of  choice is surgical excision

• Excise widely because of their superficial nature

• Excise deeply in dysplastic & carcinoma in situ lesions

• Follow up examinations are critical for patients with these lesions

• Dysplastic & in situ lesions eventually become invasive

Kaposi Sarcoma

Various etiologic factors:

• Genetic predisposition

• Infection (especially viral)

• Environmental influences of various geographic regions

• Immune dysregulation - Reduced immunosurveillance

Kaposi Sarcoma

• Regarded as neoplasm

• Considered as inflammatory in nature during its early stages

• Endothelial cell in origin

• Dermal & submucosal dendrocytes may have a role in the genesis of these lesions

Kaposi Sarcoma

clinical features:

• Oral lesion may be the initial site of involvement or the only site

  • Palate is the most common site 

• From flat lesion to a rather ominous, nodular exophytic lesion

• Maybe single or multifocal 

• Color is usually red to blue

• Other oral problems may exist - Candidiasis, hairy leukoplakia, advancing periodontal disease, xerostomia

3 types of kaposi sarcoma

• classic type

• African/ endemic type

• immunodeficiency type

Classic type of kaposi sarcoma

• Rare skin lesion

• Seen in older men living in the Mediterranean basin

• Appear as multifocal reddish-brown nodules primarily in the skin of the lower extremities

• Oral lesions are rare

• Long indolent course with good prognosis

Classic type of kaposi sarcoma

affected area is skin only (type of kaposi sarcoma)

African type of kaposi sarcoma

rare in oral cavity; skin is the most affected

African type of kaposi sarcoma

• Considered endemic

• Typically seen in the extremities of blacks

• Skin is the most commonly affected organ

• Rare oral lesions

• Clinical course is prolonged

• Overall prognosis is fair

Immunodeficiency type of kaposi sarcoma

common in oral cavity (type of kaposi sarcoma)

Immunodeficiency type of kaposi sarcoma

• Seen in patients with immunodeficiency state especially AIDS

• Skin lesions are multifocal

• May affect anywhere on the skin & visceral organs

• Younger group are affected

• Oral & lymph node lesion are relatively common

• Clinical course is rapid & aggressive with poor prognosis

kaposi sarcoma table

Kaposi Sarcoma

histopathology:

• Composed of spindle cells & ill-defined vascular channels

• Atypical vascular channels, extravasated red blood cells, hemosiderin & inflammatory cells are characteristic of advanced Kaposi’s sarcoma

Kaposi Sarcoma

differential dx:

• Hemangioma

• erythroplakia

• melanoma

• pyogenic granuloma

Kaposi Sarcoma

treatment:

• Surgery for localized lesions

• Low-dose radiation & chemotherapy for larger & multifocal lesions

• Chemotherapeutic regimens include several anti-cancer drugs

1 Unknown etiology

• geographic tongue

Benign migratory glossitis

another term for geographic tongue

Geographic Tongue

• May appear as a red tongue lesion

• Often occurs in association with fissured tongue

• A component of the Melkersson-Rosenthal syndrome

• Usually asymptomatic

• Painful only if C. albicans organism colonize the base of the fissue

• looks like median rhomboid glossitis

4 Metabolic-Endocrine Conditions (intravascular,diffuse)

• vitamin B deficiencies

• pernicious anemia

• iron deficiency anemia

• burning mouth syndrome

Vitamin B Deficiencies

etiology:

• May involved individuals belong in the poor socio-economic sectors

• May involve one or several water-soluble B complex vitamin

  • Due to decreased intake through alcoholism, starvation or fad diets

  • Due to decreased absorption because of gastrointestinal disease

  • Due to increased utilization because of increased demand

Vitamin B Deficiencies

clinical features:

• General Oral changes : cheilitis & glossitis

  • Angular cheilitis- Lips exhibit cracking & fissuring that is exaggerated at the corners of the mouth

  • Tongue becomes reddened with atrophy of the papillae with pain & burning sensation

• Riboflavin deficiency results in keratitis of the eyes & a scaly dermatitis on the nasolabial area and genitalia

• Niacin deficiency is associated with extraoral problems:

  • 4 Ds: dermatitis, diarrhea, dementia & death

• Folic acid deficiency results in megaloblastic bone marrow, macrocytic anemia & gastrointestinal abnormalities

• Vitamin B12 deficiency shares many symptoms with folic acid deficiency

Angular cheilitis

Lips exhibit cracking & fissuring that is exaggerated at the corners of the mouth

glossitis

Tongue becomes reddened with atrophy of the papillae with pain & burning sensation

cheilitis and glossitis

2 general oral changes for vitamin B deficiency

Riboflavin deficiency

•  results in keratitis of the eyes & a scaly dermatitis on the nasolabial area and genitalia

Niacin deficiency

• is associated with extraoral problems:

  • 4 Ds: dermatitis, diarrhea, dementia & death

Folic acid deficiency

 results in megaloblastic bone marrow, macrocytic anemia & gastrointestinal abnormalities

Vitamin B12 deficiency

• shares many symptoms with folic acid deficiency

Vitamin B deficiencies

diagnosis:

• Based on history, clinical findings & laboratory data

Vitamin B deficiencies

treatment:

• replacement therapy should be curative

Pernicious anemia

• Essentially a deficiency of vitamin B12 (erythrocyte maturing factor or extrinsic factor)

• Results from the inability to transport vitamin B12 across intestinal mucosa because of a relative lack of a gastric substance ( intrinsic factor)

• The end result is atrophic gastritis, achlorhydria, neurologic changes, megaloblastic bone marrow & macrocytic anemia

Vitamin B12 deficiency

usually pernicious

• Usually, nutritional deficiencies affected area is tongue

Pernicious anemia

clinical features

• Affects adults of either gender

• Clinical signs: weakness, pallor, shortness of breath, difficulty in breathing & increased fatigue on exertion

• Severe cases will show CNS manifestations & GIT manifestations

• Oral manifestations: center around the tongue

  • Pain & burning

  • Red appearance due to atrophy of the papillae : Hunter’s glossitis or Moeller’s glossitis

Hunter’s glossitis or Moeller’s glossitis

Red appearance due to atrophy of the papillae

Pernicious anemia

diagnosis:

• Based on laboratory demonstration of megaloblastic, macrocytic anemia

Pernicious anemia

treatment:

• Parenteral  administration of vitamin B12 is curative for this condition

• An increased risk of the development of gastric carcinoma is associated with the chronic atrophic gastritis

Iron Deficiency Anemia

etiology:

• Due to inadequate dietary intake

• Impaired absorption due to a gastrointestinal malady

• Chronic blood loss due to such problems as excessive menstrual flow, gastrointestinal bleeding & aspirin ingestion 

• Increased demand as experienced during childhood & pregnancy

Iron Deficiency Anemia

clinical features:

• Prevalent form of anemia affecting women

• May result in brittle nails & hair & koilonychia (spoon-shaped nails)

• The tongue may become red, painful & smooth

• Angular cheilitis may also be seen

• Plummer-Vinson syndrome

  • Dysphagia, 

  • Atrophy of the upper alimentary tract  

  • Predisposition to the development of oral cancer

Iron Deficiency Anemia

differential dx:

• Laboratory blood studies

• Slight to moderate reduced hematocrit

• Reduced hemoglobin level

• RBCs are microcytic & hypochromic

• Serum iron is also low

Iron Deficiency Anemia

tx:

• Recognition of the underlying cause of iron deficiency anemia is necessary to effectively treat this condition

• Dietary iron supplements are required to elevate hemoglobin levels & replenish iron stores

Burning tongue syndrome

another term for burning mouth syndrome

Burning Mouth Syndrome

• Burning mouth or burning tongue syndrome

• Usually no clinically detectable lesions, although pain & burning can be intense

• Common “non-lesion” clinical problem

• Its symptoms also appear in vitamin B deficiency, pernicious anemia, iron deficiency anemia & chronic atrophic candidiasis

Burning Mouth Syndrome

etiology:

• Significant etiologic factors:

  • Microorganisms: esp. fungi & possibly bacteria

  • Xerostomia: Sjorgren’s syndrome, anxiety or drugs

  • Nutritional deficiencies: Vit B complex, iron, or zinc

  • Anemias: pernicious & iron deficiency anemia

  • Hormone imbalance: post-menopausal changes

  • Neurologic abnormalities: depression, cancer phobia

  • Diabetes mellitus

  • Mechanical trauma: chronic denture irritation & habit

  • Idiopathic cases

  • In some patients, more than one of the etiologic factors may be contributory to the condition

  • Other potential etiologic factors are:

    • Dysgeusia – altered taste associated with an equally long list of factors such as zinc deficiency, drugs( esp. antibiotics), endocrine abnormalities, Vincent’s infection, heavy-metal intoxiation, chorda tympani injury & psychogenic & idiopathic causes

Burning Mouth Syndrome

clinical features:

• Typically affects middle-age females

  • Males are affected at a later age

  • Rare in children & teenagers

• Pain & burning symptoms may be accompanied by altered taste & xerostomia

  • Becomes severe & ever-present or worsening late in the day & evening

  • Tongue is the most common involved site

• May also associated with a recent dental works: new bridge or extraction of tooth

Burning Mouth Syndrome

Differential dx:

• Based on detailed history, negative clinical examination, laboratory studies & exclusion of all other possible oral problems

Tx:

• Is nutritional deficit is the cause, replacement therapy will be curative

• If a patient wears a prosthetic device, careful inspection of its fit & tissue base should be done

• If fungal infection is present, topical nystatin or clotrimazole therapy

• If drugs is the cause, alternative drugs may be beneficial

Infectious conditions

• scarlet fever

• atrophic candidiasis

Scarlet Fever

etiology:

• Result of an erythrogenic toxin produced by some strain of group A streptococci  that causes capillary damage

• Spread is via droplets from contact with an infected individual or a carrier

• Crowded living conditions promote the spread of streptococcal infections

Scarlet fever

clinical features

• Children are typically affected

•  Incubation period of several days

• Usual symptoms:

  • Pharyngitis

  • Tonsillitis

  • Fever

  • Lymphadenopathy

  • alaise

  • Headache

  • Red skin rash - Starts on the chest & spread to other surfaces

• Face is flushed except for a zone of circumoral pallor

• Palate may show inflammatory changes

• Tongue may become covered with a white coat in which the fungiform papillae are enlarged & reddened (strawberry tongue)

• Later, the coat is lost, leaving a beefy red

• tongue (red strawberry tongue or raspberry tongue)

• Uncomplicated cases subsided in a matter of days even untreated one

• Complications of pharyngeal suppuration (abscesses), direct extension to adjacent structures & metastatic infection occasionally be seen

• Non-suppurative hypersensitivity complications of rheumatic fever & glomerulonephritis are also important potential problems

Scarlet fever

diff dx:

• Staphylococcus aureus infections, viral infections & drug eruptions

• Definitive diagnosis is based on history, clinical presentation & throat culture

tx:

• Penicillin is the drug of choice

• Erythromycin should be used in patients allergic to penicillin

• Rationale for antibiotic treatment of this short- lived, self-limited disease

• Prevention of complications especially rheumatic fever & glomerulonephritis

Atrophic Candidiasis

• Caused by Candida albicans

• Opportunistic infections

Atrophic Candidiasis

clinical features

• Acute atrophic candidiasis follows the loss of the white fungal colonies from the surface of the mucosa

• The lesion is red & painful

• Chronic atrophic candidiasis also appears as a red, painful lesion, typically under a maxillary denture or commissure of the mouth

Immunologic abnormalities

• plasma cell gingivitis

• Drug Reaction and Contact Allergies

plasma cell gingivitis

• An allergic or hypersensitive reaction Ingredient in chewing gum such as mint or cinnamon flavorings

• Rarely seen today, numerous cases seen in the early 1970s

clinical features

• Affects adults & occasionally children of either gender

• Symptoms: burning mouth, tongue or lips

• Onset is sudden & discomfort can wax and wane Attached gingiva is fiery red but not ulcerated Tongue is atrophic & red

• Commissure of the lips are reddened, cracked & fissured

histopath:

• Affected epithelium is spongiotic & infiltrated by various types of inflammatory cells 

• Langerhans cells are also prominents 

• Infiltration of plasma cell

plasma cell gingivitis

diff dx:

• Triad of gingivitis, glossitis & angular cheilitis are diagnostic

• If the tongue & commissure changes are prominent, vit B deficiency or anemia will have to be considered

• If gingival changes are more prominent, the following will have to be considered

• DLE, atrophic lichen planus, psoriasis, cicatricial pemphigoid, contact allergic reaction

tx:

• Cessation of gum chewing

• In non-gum chewers or those who do not respond to the cessation of gum chewing:

  • Careful dietary history taking to find out the identity of the allergic source

Drug Reaction and Contact Allergies

• Drugs taken systemically or used topically

• Clinical appearance in the skin & oral mucosa:

  • Red erythematous lesion, urticarial rash, vesiculo- ulcerative eruption

clinical features

• Skin and oral mucosa: Red erythematous lesion, urticarial rash, vesiculo-ulcerative eruption