Characterization of juvenile spongiotic gingival hyperplasia as an entity of odontogenic origin

• Published in: Journal of periodontology (1970) Vol. 90; no. 12; p. 1490
• Main Authors: Lafuente-Ibáñez de Mendoza, Irene, Alberdi-Navarro, Javier, Marichalar-Mendia, Xabier, Mosqueda-Taylor, Adalberto, Aguirre-Urizar, Jose Manuel
• Format: Journal Article
• Language: English
• Published: United States 01.12.2019
• Subjects: Adolescent; Child; Epithelial Attachment; Epithelium; Female; Gingiva; Gingival Hyperplasia; Humans; Hyperplasia; Male; junctional epithelium; gingival hyperplasia; cytokeratin; odontogenic tumor
• DOI: 10.1002/JPER.19-0022

Juvenile spongiotic gingival hyperplasia (JSGH) is a distinct clinicopathological entity of the buccal gingiva of young patients which has been related to several factors such as plaque formation, hormonal modifications, and viral infections; however, its true etiopathogenesis remains unsolved. Several immunohistochemical studies have demonstrated the similarity between the junctional epithelium (JE) and the hyperplasic epithelium of JSGH. The objective of this study is to analyze the clinicopathological and immunohistochemical characteristics of JSGH to explain its origin. Clinicopathlogical data of 10 cases of JSGH (five men and five women) with a mean age of 13 years (range: 9 to 17 years) were collected. CK7, CK14, CK19, CD3, CD20, S100, and Ki-67 antibodies were used for comparative immunohistochemical study. All the lesions showed hyperplasic epithelium in its central portion, exhibiting marked spongiosis, vascular proliferation, and a chronic inflammatory infiltrate on the subepithelial connective tissue. CK19 was positive in the whole hyperplasic epithelium of JSGH and the basal layer of the marginal gingiva, while expression of CK14 was present in all epithelial layers of both the JSGH and that of the marginal gingiva. The subepithelial inflammatory infiltrate has a larger amount of CD20 positive cells. JSGH is a reactive tumor of the gingiva that may have an odontogenic etiology, whose origin seems to be the remnants of JE.