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Oral Hemangiomas Clinical Presentation

  • Author: Steven Brett Sloan, MD; Chief Editor: William D James, MD  more...
Updated: Feb 09, 2016


Hemangiomas and vascular malformations are diagnosed fairly easily with a careful history and a physical examination.

Capillary hemangiomas are usually not present at birth but are antedated by a pale, well-demarcated, flat area, most visible with agitation. These prodromal lesions may appear as a pale halo surrounding an area of telangiectasis or as a very fine telangiectasia similar to the port-wine stain.

Elevation occurs early during the first year of life and increases from the ages of 3-8 months, with some growth continuing into the second year of life. A stable interval of 6-12 months often follows the growth period. Then, a slow spontaneous involution, which usually begins in the center of the lesion, takes place in most cases. Involution often begins as a darkening of color followed by the appearance of numerous gray or pallid regions and fibrous septae within the lesion. Historically, most lesions have reportedly involuted by the time the patient is aged 7 years, with 86% of those lesions regressing by the time the patient is aged 5 years.[19, 20, 21, 18, 22]

The patient's sex and the size of the hemangioma do not influence the speed or the completeness of resolution. The location of the lesion does not generally influence its behavior, but lesions of the lower lip are less favorable. Patients with multiple lesions have rates of resolution similar to those with single lesions; however, separate lesions in the same individual do not necessarily grow or involute simultaneously. Lesions that have not improved after 3 years are unlikely to resolve by age 7 years. Unfortunately, early improvement does not always lead to early resolution. Involution may continue into the late teenage years.

Cavernous hemangiomas are composed of large, irregular, deep dermal and subcutaneous blood-filled channels that impart a purplish discoloration to the overlying skin. They are typically soft, poorly defined, and readily blanch with compression, giving them a characteristic "bag of worms" feel. The lesion may expand and darken with crying, when agitated, or when placed in a dependent position. Often, a capillary component overlies a cavernous component, and it may be difficult to distinguish these components histologically. Cavernous and mixed hemangiomas demonstrate the same patterns of proliferation as those of capillary lesions. However, involution is often incomplete, depending on the location and the presence of associated arteriovenous malformations.

Vascular malformations are present at birth and continue to grow with the child. The growth may become accelerated when the patient undergoes puberty or pregnancy, with the attendant hormonal changes.



On examination of the oral cavity, the vascular malformations of the mucosa and the adjacent soft tissues are usually readily apparent. The tissues have a slightly bluish hue and are soft. Venous channels become engorged when placed in a dependent position. They are readily compressible and fill slowly when released. They lack a prominent pulsation; if they represent an arteriovenous malformation, a thrill may be present.

Although the mucosal and soft tissue lesions are readily suspected by their appearance, the intrabony lesions may be difficult to distinguish on sight alone. Central jaw lesions can show hypermobility of the teeth and distortion of the arch form.[12] Severe hemorrhage following dental extraction is not an uncommon presentation of central hemangiomas of the maxilla and the mandible.[17] Common clinical findings in central hemangiomas of the jaws include gingival bleeding, postextraction bleeding, swelling, pain, mobility of the teeth, and bony expansion.[17] Root resorption of the teeth has been reported in 30% of cases, but the vitality of the teeth is usually not affected.[12]

Intramuscular vascular malformations represent a challenge on diagnosis because they exhibit few signs on clinical examination. Oftentimes, the extent of the lesion is not clinically apparent on examination, and imaging studies frequently define more extensive lesions than suspected.



The causes of vasoformative tumors are unknown. One hypothesis postulates that placental cells, such as the trophoblast, may be the cell of origin for hemangiomas. Therefore, hemangiomas may arise secondary to some event in utero. However, conflicting evidence supports this hypothesis. One study found placenta-associated vascular antigens to be expressed by hemangiomas but not by other vascular malformations or tumors. On the other hand, a separate investigation found immunohistochemical staining of certain trophoblastic markers to be negative in all infantile hemangiomas that were examined. The relationship between hemangiomas and placental tissues needs further investigation.

Contributor Information and Disclosures

Steven Brett Sloan, MD Associate Professor, Department of Dermatology, University of Connecticut School of Medicine; Residency Site Director, Connecticut Veterans Affairs Healthcare System; Assistant Clinical Professor, Yale University School of Medicine

Steven Brett Sloan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, Connecticut State Medical Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Journal of the American Academy of Dermatology;Up to Date;Medical Review Institute of America.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: American Medical Association, Alpha Omega Alpha, Association of Military Dermatologists, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Phi Beta Kappa

Disclosure: Nothing to disclose.

Drore Eisen, MD, DDS Consulting Staff, Department of Dermatology, Dermatology Research Associates of Cincinnati

Drore Eisen, MD, DDS is a member of the following medical societies: American Academy of Dermatology, American Academy of Oral Medicine, American Dental Association

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Neil Shear, MD Professor and Chief of Dermatology, Professor of Medicine, Pediatrics and Pharmacology, University of Toronto Faculty of Medicine; Head of Dermatology, Sunnybrook Women's College Health Sciences Center and Women's College Hospital, Canada

Neil Shear, MD is a member of the following medical societies: Canadian Medical Association, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada, Canadian Dermatology Association, American Academy of Dermatology, American Society for Clinical Pharmacology and Therapeutics

Disclosure: Nothing to disclose.


Randall Wilk, MD, DDS, PhD Associate Professor, Department of Oral and Maxillofacial Surgery, Louisiana State University Health Science Center

Randall Wilk, MD, DDS, PhD is a member of the following medical societies: American Association of Oral and Maxillofacial Surgeons, American Dental Association, and American Medical Association

Disclosure: Nothing to disclose.

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Table 1. Classification of Vasoformative Tumors
Vasoformative Tumor New Nomenclature Old Nomenclature
  Capillary hemangioma Strawberry hemangioma
    Juvenile hemangioma
  Cavernous hemangioma  
  Mixed hemangioma Parotid hemangioma
Vascular malformations    
  Venous malformation Cavernous hemangioma
  Intramuscular venous malformation Intramuscular hemangioma
  Capillary malformation Capillary hemangioma
    Port-wine stain
  Arteriovenous malformation Arteriovenous hemangioma

Arterial angioma

Arteriovenous aneurysm

Cirsoid angioma

Red angioma

Serpentine aneurysm

  Lymphatic malformation Capillary lymphangioma

Cavernous lymphangioma


Cystic hygroma

Table 2. Complications From Ablative Surgery Following Embolotherapy or Sclerotherapy for Hemangiomas and Vascular Malformations
Complications Hemangiomas, % Vascular Malformations, %
Immediate Complications
Hemorrhage 27 60
Airway compromise 2 10
Hematoma 14 14-30
Skin necrosis 12 10-30
Coagulopathy 7 14-20
Late Complications
Restricted oral opening 8 27-40
Malocclusion 8 20-40
Drooling 23 40-47
Dysphagia 23 20-27
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