Pyogenic Granuloma of the Oral Cavity: Clinical and Histopathological Features, Etiopathogenesis, and Management
How to cite this article: Aoun G. Pyogenic Granuloma of the Oral Cavity: Clinical and Histopathological Features, Etiopathogenesis, and Management. J Health Sci Res 2023;8(1):26-28.
Pyogenic granuloma (PG) refers to a non-malignant vascular tumor that usually arises on the skin and mucous membranes. In the oral cavity, the gingiva is the most commonly affected. PG may result from minimal local irritation, chronic trauma, and changes in hormones. It can be found at all ages, especially during the 2nd–5th decades of life. It is more likely to occur in females in whom the hormones estrogen and progesterone are high. This article reviews the clinical and histopathological features of oral PG, as well as its etiopathogenesis, differential diagnosis, and treatment.
Pyogenic granuloma (PG), also called lobular capillary hemangioma, is a non-malignant vascular tumor that usually affects the skin and mucous membranes, mostly of the oral cavity, and can rarely be found subcutaneously or intravascularly1. In rare cases, it may arise elsewhere within the gastrointestinal tract. This is an inflammatory hyperplasia resulting from chronic irritants, including trauma, changes in hormones, or certain medications such as oral contraceptives, retinoids, and anticancer drugs2-4. Oral PG belongs to a group of nodular growths located in the mucosa with histologic features including inflamed fibrous and granulomatous tissue. This group also includes epulis fissuratum, palatal papillary hyperplasia, and pregnancy tumors5. The aim of this article is to review the clinical and histopathological features, the etiopathogenesis, the differential diagnosis, and the treatment of oral PG.
Clinically, oral PG may appear as a pedunculated exophytic overgrowth that is extremely soft in consistency. It bleeds easily and has a smooth and shiny overlying mucosa. Oral PG may also manifest as a sessile plaque6,7. The lesion is usually painless, measuring a few millimeters to a few centimeters. It reaches its full size in a few weeks or months8. In 75% of the cases, oral PG is located in the gingiva, especially in the interdental space in the maxillary anterior region (Figure 1). It may also affect the lips, the tongue, the buccal mucosa, and the palate9.
Oral PG typically presents histopathologically as a well- defined lesion composed of vascular sections bordered by normal endothelium. The connective tissue is infiltrated by polymorphic leukocytes. The squamous epithelium is invaginated at the edge of the lesion and ulcerated on the surface. While tumor cells are absent, parakeratosis may be noted16.
The exact etiology of PG remains unknown14,17. This non-neoplastic inflammatory hyperplasia was once thought to be a bacterial or fungal infection, but it is actually believed to be an inflammatory process reaction associated with exuberant fibrovascular proliferation of the connective tissue2,5,14,17. Various factors are suggested to be implicated in the etiopathogenesis of PG, such as chronic low-level local irritation from overhanging restorations or calculus, trauma, hormonal changes, bone marrow transplants, reactions to grafts, and certain drugs, including calcium channel antagonists, immunosuppressants, antiseizure drugs, and anticancer medications. Among the latter are “TNF-α antagonists, BRAF inhibitors, tyrosine kinase inhibitors, epidermal growth factor receptor inhibitors, mTOR inhibitors, taxanes, and pyrimidine analogs14,18.”
Oral PG is primarily considered to be connected to pregnancy. According to Kanda and Watanabe19, “estrogen improves the production of vascular endothelial growth factor in macrophages, leading to the development of PG.” In addition, in their study, Ojanotko-Harri et al.20 concluded that “during pregnancy, progesterone may operate as an immunosuppressant in the gingiva, thus preventing an acute inflammatory response against bacteria and resulting in proliferative gingival inflammation.”
Differential diagnosis of PG includes peripheral giant cell granuloma, peripheral ossifying fibroma, Kaposi sarcoma, and metastatic cancer2,17. All these lesions may be clinically identical to PG and must be differentiated based on histopathologic examination.
Oral PG is surgically excised to periosteum depth and within 2–3 mm of the clinical limits, followed by curettage of the underlying tissue. The possible causative factors must certainly be removed. During surgery, vigilant monitoring is important because of the vascular nature of the lesion, which leads to abundant bleeding17. Recurrence after excision has been reported to occur in up to 16% of cases, with gingival PG presenting an elevated recurrence rate14,21. Other surgical techniques that have been used for the treatment of PG include “cryosurgery using liquid nitrogen or a cryoprobe, and laser therapy by means of diode lasers of wavelength 808 to 980 nm, neodymium: yttrium-aluminum-garnet (Nd: YAG), and CO2 lasers7,21-26.” Sclerotherapy consisting of intralesional injections of ethanol and sodium tetradecyl sulfate was also suggested8,27.
PG is a non-neoplastic lesion with an unidentified etiology. In the oral cavity, its diagnosis is challenging, and recurrence after surgical treatment is highly reported. Therefore, their early and accurate diagnosis and treatment, along with regular postoperative follow-ups, are obligatory for best treatment outcome and recurrence prevention.