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Pyogenic granuloma (Lobular capillary hemangioma)

Leslie P Lawley, MD
Section Editor
Moise L Levy, MD
Deputy Editor
Rosamaria Corona, MD, DSc


Pyogenic granuloma (PG) or lobular capillary hemangioma [1] is a benign vascular tumor of the skin or mucous membranes characterized by rapid growth and friable surface. PG occurs at any age, although it is seen more often in children and young adults. Surgical treatment is usually required because PG rarely resolves spontaneously and often bleeds repeatedly and profusely.

This topic will discuss the pathogenesis, clinical manifestations, diagnosis, and treatment of pyogenic granuloma. Other benign and malignant vascular tumors are discussed separately. (See "Infantile hemangiomas: Epidemiology, pathogenesis, clinical features, and complications" and "Rapidly involuting congenital hemangioma (RICH) and noninvoluting congenital hemangioma (NICH)" and "Classic Kaposi sarcoma: Clinical features, staging, diagnosis, and treatment" and "AIDS-related Kaposi sarcoma: Staging and treatment".)


Pyogenic granuloma (PG) occurs in patients of all ages with a peak incidence in the second and third decades of life [2,3]. In children, the average age at diagnosis is 6 to 10 years and there is a predilection for males [3-5]. Mucosal PG is more common in adult women than in men or children [6,7]. About 2 percent of pregnant women develop an intraoral PG in the first five months of pregnancy [8]. (See "Maternal adaptations to pregnancy: Skin, hair, nails, and mucous membranes", section on 'Vascular tumors'.)


Although the name suggests an infectious etiology, the cause of pyogenic granuloma (PG) is unknown. Most theories on pathogenesis revolve around PG as a hyperplastic, neovascular response to an angiogenic stimulus with imbalance of promoters and inhibitors [3,9]. Angiogenic growth factors such as vascular endothelial growth factor (VEGF) and decorin, transcription factors (pATF2 and pSTAT3), and mitogen-activated protein kinase (MAPK) signal transduction pathway proteins are overexpressed in PGs, but their exact role is undetermined [9-11]. A whole-exome sequencing study of 40 PG lesions found HRAS somatic mutations in four tumors, supporting a role for the RAS-MAPK pathway in the development of PG [12]. An analysis of 11 PGs revealed embryonic stem cell markers in the endothelial cells and a more differentiated pattern in the interstitial cells suggesting de novo vasculogenesis from the primitive stem cells [13].

Trauma has been suggested as a trigger, although only 7 to 23 percent of patients with PG report a previous injury at the site [4,5]. In a series of patients with periungual or subungual PG, local injury (eg, acute mechanical trauma, onycholysis, or chronic nail manipulation) was reported in 58 percent of cases [14]. Patients who have undergone hematopoietic cell transplant have been reported to develop mucosal PG thought to be related to the trauma of oral graft-versus-host disease or medications taken post-transplant [15].

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Literature review current through: Oct 2017. | This topic last updated: Oct 11, 2017.
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