Pyogenic granuloma (lobular capillary hemangioma  ) is a relatively common benign vascular lesion of the skin and mucosa whose exact cause is unknown. Also see the Medscape Reference article Oral Pyogenic Granuloma.
Pyogenic granulomas are misnamed; they are neither infectious nor granulomatous. The lesion usually occurs in children and young adults as a solitary, glistening red papule or nodule that is prone to bleeding and ulceration. Pyogenic granulomas typically evolve rapidly over a period of a few weeks, most often on the head, neck, extremities, and upper trunk.
Pyogenic granuloma often arises in pregnancy (or rarely with oral contraceptive usage), particularly on the gingiva or elsewhere in the oral mucosa, and then is termed the "pregnancy tumor."
Other pyogenic granuloma variants that have been well documented include the disseminated, subcutaneous, intravenous, and medication-induced (for example, retinoid, antiretroviral, and oncologic agent) subtypes.
Removal of pyogenic granuloma is indicated to alleviate any bleeding, discomfort, cosmetic distress, and diagnostic uncertainty. A number of malignant tumors may clinically mimic pyogenic granuloma, making histopathologic confirmation important if the presentation is atypical.
Aside from cutaneous and oral lesions, pyogenic granuloma has been reported throughout the gastrointestinal tract and upper airway, at various ocular locations, the central nervous system, the bladder, and the internal vasculature. This article discusses only cutaneous and oral involvement.
The precise mechanism for the development of pyogenic granuloma (lobular capillary hemangioma) is unknown. Trauma, hormonal influences, certain medications, viruses, underlying microscopic arteriovenous malformations, the production of angiogenic growth factors, and cytogenetic abnormalities have all been postulated to play a role. The overexpression of transcription factors P-ATF2 and STAT3 also may play a role in tumorigenesis.  Endothelial nitric oxide synthases (eNOS), CD34, and CD105/endoglin expression are markers of angiogenesis in pyogenic granulomas. [3, 4] . Tissue injury may trigger pathologic angiogenesis driven by FLT4, a tyrosine-kinase receptor, and the nitric acid pathway.  COX-2 and IL-10 may be involved in the etiopathogenesis of oral pyogenic granulomas.  BRAF and RAS mutations have been identified, suggesting a true neoplastic process. [7, 8]
International frequency for pyogenic granuloma is likely similar to that of the United States.
The frequency of pyogenic granuloma appears to be similar in all races.
Pyogenic granulomas are equally prevalent in male and female patients, though oral mucosal lesions are twice more common in females, likely due to the pregnancy tumor phenomenon. 
Pyogenic granuloma is rare in children younger than 6 months. The peak age of onset for cutaneous lesions is the second decade of life.  For patients younger than 17 years, the mean age of presentation has been reported as 6.7 years.  Aside from those lesions occurring in pregnancy, the frequency declines linearly with age in adulthood. Also see the Medscape article, Pediatric Pyogenic Granuloma.