RED-BLUE LESIONS & PIGMENTED LESIONS

A set of practice questions covering red-blue lesions and pigmented lesions from the lecture notes, including congenital lesions, reactive vascular lesions, infectious mimics, pigmented mucosal disorders, and related systemic associations.

What are the two main categories referred to by terms like congenital hemangioma and congenital vascular malformation?

Congenital hemangiomas (strawberry nevus) and congenital vascular malformations.

Which congenital lesion is commonly known as strawberry nevus?

Congenital hemangioma.

What growth pattern is typical of congenital hemangiomas?

A rapid growth phase followed by involution.

Do congenital vascular malformations typically involute during childhood?

No, they generally do not involute; they persist and grow with the individual.

Where are congenital vascular lesions most commonly found in the oral region?

Lips, tongue, and buccal mucosa.

When affecting the mandible or maxilla, what radiographic pattern is expected for these lesions?

A radiolucent lesion with a honeycomb pattern and distinct margins.

What imaging modality is definitive for lesion identification and characterization?

Angiography or angiographic magnetic resonance imaging (MRI).

Sturge-Weber syndrome is also known as what?

Encephalotrigeminal angiomatosis; a noninherited neurocutaneous syndrome with facial and leptomeningeal vascular malformations.

Which structures are typically involved in Sturge-Weber syndrome?

Venous malformations of the leptomeninges of the cerebral cortex and facial vasculature.

What is a key feature of hereditary hemorrhagic telangiectasia (HHT)?

Autosomal-dominant disorder with telangiectatic vessels and frequent epistaxis.

Where do telangiectatic vessels commonly appear in HHT?

On the face, chest, and oral mucosa.

What is a venous varix (varicosity)?

An acquired focal dilation of a single vein, common in the oral mucosa and lips.

How do ventral tongue varices typically present clinically?

As blue lesions that blanch with compression.

When is treatment indicated for varices?

Only if frequently traumatized or cosmetically objectionable.

What characterizes other acquired vascular malformations beyond simple varices?

They involve a network or proliferation of thin-walled vessels and are common in adults; may be red-blue, discrete, and easily excised.

What is the etiology of a Pyogenic Granuloma (PG)?

Exuberant connective tissue proliferation in response to a known stimulus or injury.

Where do PG lesions most commonly occur?

On the attached gingiva (about 75%).

What pregnancy-related lesion is associated with PG?

Pregnancy tumors; gingival PG lesions related to hormonal changes during pregnancy.

Describe the clinical features of a pyogenic granuloma.

Red, smooth or lobulated, hemorrhagic, compressible mass; often ulcerated; may be pedunculated or broad-based; size ranges from millimeters to several centimeters.

What is the histopathology of pyogenic granuloma?

Lobular masses of hyperplastic granulation tissue with prominent capillaries and inflammatory cells; scarring may be seen in some cases.

What triggers a peripheral giant cell granuloma (PGCG)?

Local trauma or irritation causing reactive hyperplasia of gingival connective tissue.

Where is PGCG typically located?

Gingiva, usually between the first permanent molars and incisors.

What histologic feature is characteristic of PGCG?

Multinucleated giant cells within a fibroblastic stroma; giant cells resemble osteoclasts.

How is PGCG treated?

Surgical excision with removal of local irritants; recurrence can occur if periosteum or periodontal ligament are not included.

What causes scarlet fever?

Exotoxin-producing group A Streptococcus (A, B, or C).

What tongue feature is associated with scarlet fever?

Strawberry tongue; white coating with enlarged red fungiform papillae that later redden.

What is erythroplakia?

A red patch on oral mucosa not a specific microscopic diagnosis, often with severe dysplasia or carcinoma.

Where are erythroplakia lesions most commonly found?

Floor of the mouth, tongue, retromolar mucosa, and soft palate.

What proportion of erythroplakias show severe dysplasia or carcinoma?

About 40% with severe dysplasia; ~50% with squamous cell carcinoma; ~9% with mild/moderate dysplasia.

How should erythroplakia be treated?

Surgical excision with adequate margins; margins should be sufficiently deep; multiple histologic sections may be needed; close follow-up.

What etiologic agent is linked to Kaposi sarcoma?

Human herpesvirus 8 (HHV-8, KSHV).

What are the three clinical patterns of Kaposi sarcoma?

Classic form, endemic African form, and immunodeficiency-associated form (AIDS-related).

Which oral sites are commonly affected by Kaposi sarcoma?

Palate, gingiva, and tongue.

What are typical histopathologic features of Kaposi sarcoma?

Early lesions show bland spindle cells and ill-defined vascular channels; extravasated RBCs; later lesions resemble pyogenic granuloma; HHV-8 immunostaining aids diagnosis.

What are common clinical features of Vitamin B deficiencies in the mouth?

Cheilitis and glossitis, angular cheilitis, tongue atrophy, burning pain.

What is the etiology of pernicious anemia?

Vitamin B12 deficiency due to lack of intrinsic factor from autoimmune attack on gastric parietal cells.

What are oral signs of pernicious anemia?

Glossitis with a red, smooth tongue (Hunter's or Moeller's glossitis); painful burning sensation.

How is pernicious anemia diagnosed?

Laboratory evidence of megaloblastic, macrocytic anemia.

What are common features of iron deficiency anemia?

Microcytic, hypochromic RBCs; low serum iron; elevated TIBC; menstruation- or pregnancy-related risk in women; may have brittle nails and angular cheilitis.

What is the diagnostic pattern for iron deficiency anemia on labs?

Low hematocrit/Hgb, microcytosis, low iron, high TIBC.

How is iron deficiency anemia treated?

Dietary iron supplementation; address underlying causes.

What etiologies are grouped under Burning Mouth Syndrome (BMS)?

Infectious (Candida, bacteria), xerostomia, nutritional deficiencies, anemia, hormonal imbalance, neuropsychiatric factors, diabetes, and mechanical trauma.

Which demographic is most commonly affected by BMS?

Middle-aged women; rare in children; may worsen in the evening; teeth and oral mucosa often appear normal.

How is BMS diagnosed?

Clinical diagnosis of exclusion based on history, exam, labs, and ruling out other conditions.

What are petechiae and ecchymoses in the oral cavity usually caused by?

Trauma or blood dyscrasias (e.g., leukemia, platelet/clotting disorders); appearing as red to purple spots.

What is an amalgam tattoo and how does it arise?

Focal argyrosis or amalgam tattoo is caused by iatrogenic deposition of amalgam particles in soft tissues, often after dental procedures.

How can amalgam tattoo be distinguished from melanoma?

History, symmetry/uniformity, radiographs to detect amalgam, and biopsy if uncertain.

What is the general management for amalgam tattoos?

No treatment required as they are benign; monitor and biopsy if suspicious.

What drugs are known to cause oral pigmentation besides tetracycline?

Aminoquinolines (chloroquine), cyclophosphamide, amiodarone, zidovudine (AZT), quinacrine, clofazimine, and heavy metal compounds.

What patterns does tetracycline-associated pigmentation show?

Diffuse pigmentation in sun-exposed areas; focal deposits around legs and periorbital areas; pigmentation in gums and palate.

What metals can cause oral pigmentation?

Arsenic, bismuth, platinum, lead, and mercury; deposition often along gingival margins.

What safety measures are recommended to reduce mercury exposure in dentistry?

Sealed mercury storage, sulfur dust for spills, hard floor surfaces, well-ventilated spaces, keeping amalgam scraps under water, sealed capsules, and using water spray and suction when grinding.

What is the Laugier-Hunziker syndrome?

Acquired pigmentary disorder with lip, oral, or fingernail macules and subungual melanocytic streaks.

What is Bandler syndrome?

Oral melanotic macules associated with intestinal hemangiomas.

What are the histopathologic features of oral melanoacanthoma?

Proliferation of dendritic melanocytes in an acanthotic epithelium with hyperkeratosis; S-100, Melan-A, and HMB45 positive.

What is the recommended treatment for oral melanocytic nevi?

All suspected oral nevi should be excised.

What is the typical growth pattern of oral melanoma?

Two subtypes: invasive (vertical growth) and in situ (junctional growth phase).