Oral surgery, oral medicine, oral pathology and oral radiology · 2025
Spongiotic gingival hyperplasia: identifying new mechanisms and a survey of clinical approach.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Ошибки и ограничения
История · было → стало
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Lin Justin, Jeong Will, Dempster Laura, Chugh Deepika, Posluns James, Magalhaes Marco
Аннотация
OBJECTIVE: Spongiotic gingival hyperplasia (SGH) or localized juvenile spongiotic gingival hyperplasia (LJSGH) is a rare, benign, soft tissue oral lesion that shares overlapping clinical characteristics with more common reactive gingival lesions found in adolescents. SGH is clinically unrelated to the accumulation of plaque, and treatment by periodontal debridement and improved oral hygiene measures are ineffective. Currently, the etiology and pathogenesis of SGH are unknown. The objectives of this study are: (1) to assess the ability of clinicians to recognize and manage SGH compared with other gingival lesions, and (2) to identify the underlying mechanisms of SGH pathogenesis using messenger RNA (mRNA) sequencing.
STUDY DESIGN: Orthodontic clinicians were surveyed using 4 representative clinical images (SGH, pyogenic granuloma, plaque-induced gingivitis, and squamous cell carcinoma). RNA was extracted from 3 cases of SGH and 2 cases of gingival inflamed fibromas (control), followed by differential gene expression analyses.
RESULTS: There is limited awareness among clinicians regarding SGH. Expression analyses revealed that SGH is characterized by overexpression of members of the IL-17 and TNF pathways, among others. Pathway analyses revealed upregulation of genes associated with angiogenesis, neutrophil activation, cell proliferation, and apoptosis, along with downregulation of pathways associated with keratinization.
CONCLUSIONS: Increased education focused on oral pathology may be beneficial and bring more awareness to this unique entity. Genetic analyses suggest a reactive origin, with unique IL-17 and TNF activation and proliferative pathways driving SGH growth even in the absence of plaque, and further studies are needed to generate specific treatments targeting these immune pathways.
STUDY DESIGN: Orthodontic clinicians were surveyed using 4 representative clinical images (SGH, pyogenic granuloma, plaque-induced gingivitis, and squamous cell carcinoma). RNA was extracted from 3 cases of SGH and 2 cases of gingival inflamed fibromas (control), followed by differential gene expression analyses.
RESULTS: There is limited awareness among clinicians regarding SGH. Expression analyses revealed that SGH is characterized by overexpression of members of the IL-17 and TNF pathways, among others. Pathway analyses revealed upregulation of genes associated with angiogenesis, neutrophil activation, cell proliferation, and apoptosis, along with downregulation of pathways associated with keratinization.
CONCLUSIONS: Increased education focused on oral pathology may be beneficial and bring more awareness to this unique entity. Genetic analyses suggest a reactive origin, with unique IL-17 and TNF activation and proliferative pathways driving SGH growth even in the absence of plaque, and further studies are needed to generate specific treatments targeting these immune pathways.