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Localized juvenile spongiotic gingival hyperplasia featuring unusual p16 INK 4A labeling and negative human papillomavirus status by polymerase chain reaction
Author(s) -
Argyris Prokopios P.,
Nelson Andrew C.,
Papanakou Styliani,
Merkourea Stavroula,
Tosios Konstantinos I.,
Koutlas Ioannis G.
Publication year - 2015
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.12214
Subject(s) - pathology , polymerase chain reaction , lesion , medicine , pathogenesis , hyperplasia , immunostaining , hpv infection , immunohistochemistry , biology , cancer , gene , biochemistry , cervical cancer
Background Localized juvenile spongiotic gingival hyperplasia ( LJSGH ) is a distinct type of gingival hyperplastic lesion with specific clinicopathologic features. Evaluation of the morphological characteristics of LJSGH indicates the potential role of human papillomavirus ( HPV ) infection as an underlying etiopathogenetic mechanism. Methods All cases of LJSGH from 2008 to present were retrieved. Clinical and demographic data were collected. HPV status was investigated by p16 INK 4A immunohistochemistry and HPV ‐Polymerase chain reaction ( PCR ). Results Twenty‐one cases of LJSGH were identified, 14 (66.7%) affecting males and seven (33.3%) females (M:F = 2:1, age range: 8–36, mean: 13 years). All lesions were well‐demarcated, exophytic, erythematous, and hemorrhagic with granular or slightly papillary surface. Preponderance for the maxillary gingiva (19, 90.5%) was observed. Two (9.5%) patients presented with recurrence 20 and 21 months after excision (mean follow‐up: 18.7 months). Histopathologically, all LJSGH lesions featured epithelial hyperplasia with intense neutrophilic exocytosis and spongiosis. All cases demonstrated positivity for p16 INK 4A with the majority of specimens (47.6%) intensely decorated in >50% of the overlying epithelium with focal immunostaining observed in 47.6% and diffuse in 52.4%. Thirteen cases (61.9%) were negative for HPV DNA by PCR , while two (9.5%) were suspicious for the presence of low levels of HPV DNA but definitive genotyping was not possible. One case (4.8%) displayed positivity for HPV ‐31. The remaining five cases failed the PCR reaction. Conclusions Human papillomavirus does not participate in the pathogenesis of LJSGH . P16 INK 4A expression in the absence of detectable HPV DNA can likely be attributed to the intense inflammation associated with LJSGH .