Oral red lesions

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