This document provides information on various oral red lesions, including their etiology, clinical presentation, diagnosis, differential diagnosis, and prognosis. It describes conditions such as ecchymosis, erythroplakia, fissured tongue, hemangioma, hereditary hemorrhagic telangiectasia, petechiae, plasma cell gingivitis, pyogenic granuloma, varices, and Kaposi's sarcoma. For each lesion, it outlines the potential causes, common signs and symptoms, diagnostic process, important distinctions from other diseases, and typical outlook. The goal is to educate medical professionals on interpreting and managing different types of red lesions in the oral cavity.

1. Oral Red Lesions
ASST. PROF. DR. GÜRKAN ÜNSAL

2. Learning Outcomes
• Explains the etiology of the lesions
• Interprets the clinical picture of the lesions
• Knows the necessary tests for the diagnosis of the lesions
• Makes a differential diagnosis of the red lesions
• Describes the prognosis of the lesions

3. LIST OF LESIONS
❑Ecchymosis*
❑Petechiae*
❑Erythroplakia*
❑Pyogenic Granuloma*
❑Hemangioma*
❑Hereditary Hemorrhagic Telangiectasia*
(Rendu-Osler-Weber Syndrome)
❑Fissured Tongue
❑Kaposi’s Sarcoma
❑Plasma Cell Gingivitis
❑Varices

4. Algorithm
❑Name of the lesion
❑Etiology
❑Clinical Presentation
❑Diagnosis
❑Differential Diagnosis
❑Prognosis

5. Ecchymosis
Definition: A small bruise caused by blood leaking from broken blood vessels into the tissues
of the skin or mucous membranes.
Etiology
• Soft tissue hemorrhage
• Blood dyscrasia with secondary thrombocytopenia, hemophilia
• Vascular wall defects
• Coagulopathy
• Trauma

6. Ecchymosis
Clinical Presentation
• Larger than pinpoint spots (ie, larger than petechiae)
• Nonvesicular, macular surface
• Lesions do not blanch with pressure
• Red to reddish blue to brown color

11. 1 to 3 cms

12. Ecchymosis
Diagnosis
• Characteristic size, color
• History
• Blood count, coagulation profile

13. Ecchymosis
Differential Diagnosis
• Hemophilia
• Kaposi’s sarcoma
• Hemangioma
• Thrombocytopenia,
• von Willebrand’s disease
• Leukemia
• Trauma

14. Ecchymosis
Prognosis
• Excellent

15. Erythroplakia
Etiology
• Unknown: a red patch that cannot be clinically attributed to another condition
• Contributing factors include tobacco use, alcohol consumption

16. Erythroplakia
Clinical Presentation
• Red, often velvety, well-defined patch(es)
• Most common on floor of mouth, retromolar trigone area, lateral tongue
• Usually asymptomatic
• May be smooth to nodular
• Chiefly in males

22. Erythroplakia
Diagnosis
• Appearance; history of tobacco/alcohol use
• Biopsy results differentiate from inflammatory and atrophic lesions

23. Erythroplakia
Differential Diagnosis
• Erythematous (atrophic) candidiasis
• Kaposi’s sarcoma
• Ecchymosis
• Contact stomatitis
• Vascular malformation
• Squamous cell carcinoma
• Geographic tongue/erythema migrans

24. Erythroplakia
Prognosis
• Fair to good depending upon microscopic diagnosis
• Almost all cases are premalignant to malignant upon initial discovery.
• Surgical excision if proven dysplastic/malignant

25. Fissured Tongue
Etiology
• Unknown
• May be hereditary
• Occurs with greater prevalence as population ages

26. Fissured Tongue
Clinical Presentation
• Multiple crenations or fissures
• May be seen in association with erythema migrans/geographic tongue
• Prominence increases with age
• Usually asymptomatic
• A component of Melkersson-Rosenthal syndrome
• May be a source of halitosis

28. Fissured Tongue
Diagnosis
• Characteristic appearance
• If symptomatic (pain, burning), may be related to the following:
◦ • Secondary candidiasis (antifungal prescription)
◦ • Idiopathic factors

29. Fissured Tongue
Differential Diagnosis
Well… You will get it ☺

30. Fissured Tongue
Prognosis
• Excellent
• With candidal colonization, topical antifungal preparations are effective.
• Careful débridement with soft-bristled brush, 5 to 15 strokes, once or twice daily

31. Hemangioma
Etiology
• Benign developmental anomalies of blood vessels that may be subclassified as congenital
hemangiomas and vascular malformations
• “Congenital hemangioma” usually noted initially in infancy or childhood (hamartomatous
proliferation)
• Congenital hemangioma due to proliferation of endothelial cells
• “Vascular malformations” due to abnormal morphogenesis of arterial and venous structures

32. Hemangioma
Clinical Presentation
• Congenital lesions usually arise around time of birth, grow rapidly, and usually involute over
several years.
• Malformations generally are persistent, grow with the child, and do not involute.
• Color varies from red to blue depending on depth, degree of congestion, and caliber of vessels
• Range in size from few millimeters to massive with disfigurement
• Most common on lips, tongue, buccal mucosa
• Usually asymptomatic
• Sturge-Weber syndrome (trigeminal encephalo-angiomatosis) includes cutaneous vascular
malformations (port wine stains) along trigeminal nerve distribution, mental retardation, and
seizures.

37. Hemangioma
Diagnosis
• Aspiration
• Blanching under pressure (diascopy)
• Imaging studies

38. Hemangioma
Differential Diagnosis
• Purpura
• Telangiectasia
• Kaposi’s sarcoma
• Other vascular neoplasms

39. Hemangioma
Prognosis
• Guarded

40. Hereditary Hemorrhagic Telangiectasia
Etiology
• Not uncommon, familial (autosomal-dominant) mucocutaneous vascular disease
• Some cases may be nonfamilial (spontaneous mutation).
• Arteriovenous (eg, pulmonary) malformations also can occur.

41. Hereditary Hemorrhagic Telangiectasia
Clinical Presentation
• Multifocal, macular to slightly papular red lesions of skin and mucosa
• Most common on lips, tongue, buccal mucosa, finger tips
• Commonly associated with epistaxis due to involvement of nasal mucosa
• Increase in number and prominence with age
• Blanch under pressure (diascopy positive)
• Lesions can affect gastrointestinal mucosa, which may rupture with associated signs of
chronic gastrointestinal blood loss; may produce anemia

45. Hereditary Hemorrhagic Telangiectasia
Diagnosis
• Family history
• Distribution of lesions

46. Hereditary Hemorrhagic Telangiectasia
Differential Diagnosis
• CREST syndrome (calcinosis cutis, Raynaud’s phenomenon, esophageal dysfunction,
sclerodactyly, telangiectasia)
• Chronic hepatitis
• Radiation-induced vascular alterations

47. Hereditary Hemorrhagic Telangiectasia
Prognosis
• Lifelong follow-up/monitoring
• 4 to 10% death rate from complications of the disease

48. Petechiae
Definition: Petechiae are pinpoint hemorrhages that occur in subcutaneous or submucosal
tissues in a wide variety of conditions. Because of their diversity, the differential diagnosis of
oral mucosal petechial hemorrhages is complex.
Etiology
• Viral infection (Epstein-Barr virus [EBV]-mononucleosis; measles), rickettsial infection
• Thrombocytopenia, leukemia
• Disseminated intravascular coagulation (DIC)
• Trauma: prolonged coughing, frequent vomiting, giving birth, violent Valsalva maneuvers

49. Petechiae
Clinical Presentation
• Pinpoint hemorrhage into mucosa/submucosa
• Asymptomatic
• Usually involves the soft palate
• No blanching on pressure (diascopy)

51. Petechiae
Diagnosis
• Clinical features
• History, determination of underlying cause

52. Petechiae
Differential Diagnosis
• See “Etiology”

53. Petechiae
Prognosis
• Variable, depending upon etiology
• Does not require treatment; observation only

54. Plasma Cell Gingivitis
Etiology
• Usually represents a hypersensitivity phenomenon to an agent such as the following:
◦ Cinnamon/cinnamon flavoring
◦ Candy flavors
◦ Toothpaste/mouthwash
◦ Plaque antigens

55. Plasma Cell Gingivitis
Clinical Presentation
• Reddened, velvety gingival surface
• Surface epithelium becomes nonkeratinized.
• Limited to attached gingiva

57. Plasma Cell Gingivitis
Diagnosis
• Response to elimination of possible etiologic agents
• Biopsy results show plasma cell infiltration within the submucosa and lamina propria beneath
an acanthotic epithelium.
• Patch testing

58. Plasma Cell Gingivitis
Differential Diagnosis
• Lupus erythematosus
• Wegener’s granulomatosis
• Chronic candidiasis
• Lichen planus
• Mucous membrane pemphigoid

59. Plasma Cell Gingivitis
Prognosis
• Reversal with removal of causative agent

60. Pyogenic Granuloma
Etiology
• A reactive hyperplasia of capillaries and fibroblasts
• Related to chronic, persistent trauma or irritation (eg, calculus or foreign body)
• Misnomer—neither pyogenic nor granulomatous
◦ My advice 🡪 Capillary Lobular Hemangioma !

61. Pyogenic Granuloma
Clinical Presentation
• Occurs at any age, but usually in children, young adults, and women
• Red, lobular to smoothly contoured appearance
• When ulcerated, a yellow fibrinous exudate covers the lesion.
• Sessile to pedunculated commonly on gingiva, but also on areas that are traumatized (eg,
lower lip, buccal mucosa)
• Bleeds easily but is painless

64. Pyogenic Granuloma
Diagnosis
• History of gradual to rapid onset
• Identification of a stimulus or causative factor (eg, trauma, physical irritant)
• Histologic evaluation

65. Pyogenic Granuloma
Differential Diagnosis
• Peripheral giant cell granuloma
• Peripheral ossifying fibroma
• Metastatic tumor
• Kaposi’s sarcoma
• Vascular malformation

66. Pyogenic Granuloma
Prognosis
• Excellent
• Recurrence occasional

67. Varices
Etiology
• An abnormal venous dilatation
• Congenital or from damage to vessel wall (trauma, ultraviolet light)
• Occur with increasing frequency over 40 years of age

68. Varices
Clinical Presentation
• Blue, lobulated surface
• Painless, evolves slowly
• Common on lower lip, sublingual regions
• Blanches with compression (diascopy)
• May become thrombosed

70. Varices
Diagnosis
• Clinical appearance
• Histologic viewing of large-caliber, thin-walled vein

71. Varices
Differential Diagnosis
• Mucocele
• Vascular neoplasm
• Blue rubber bleb nevus syndrome
• Hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber syndrome)

72. Varices
Prognosis
• Excellent

73. Kaposi’s Sarcoma
Etiology
• Several forms
◦ • Classic idiopathic form affecting extremeties
◦ • Endemic form (African)
◦ • Immunosuppression-associated form
◦ • Acquired immunodeficiency syndrome (AIDS)-associated form
• All forms, especially AIDS-associated and immunosuppressionassociated forms, may be
caused by or closely related to a herpesvirus (human herpesvirus 8 [HHV-8] or Kaposi’s
sarcoma–associated herpesvirus [KSHV]).

74. Kaposi’s Sarcoma
Clinical Presentation
• Classic form associated with slow but pernicious growth over many years; oral lesions rarely seen
• Endemic form more rapid; oral lesions rarely seen
• AIDS-associated KS most commonly seen on keratinized mucosa/mucoperiosteal tissues; strong
predilection for hard palate, followed by gingiva, buccal mucosa, and tongue (prevalence decreasing
with treatment for AIDS)
• Evolution from bluish macule to nodule(s)
• Evolution to multiple lesions
• May precede or follow cutaneous lesions
• Usually asymptomatic

77. Kaposi’s Sarcoma
Diagnosis
• Location and appearance
• May occur in up to one-third of AIDS patients
• Biopsy showing spindle cell proliferation with vascular slits, extravascular red blood cells

78. Kaposi’s Sarcoma
Differential Diagnosis
• Hematoma
• Hemangioma
• Ecchymosis
• Malignant melanoma
• Pyogenic granuloma
• Amalgam tattoo

79. Kaposi’s Sarcoma
Prognosis
• Variable, depending upon host’s immune status, but generally poor in AIDS-associated form

80. References
• Brad W. Neville, Douglas D. Damm , Carl Allen, Angela C. Chi (2015). Oral and Maxillofacial
Pathology. 4th edition, Elsevier Health Sciences, St. Louis, Missouri
• Laskaris, G. (2017). Color Atlas of Oral Diseases. 4th edition. Thieme