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Introduction <p>Ligneous gingivitis (LG) is a rare manifestation of plasminogen deficiency characterized by woody fibrin-rich pseudomembranes, recurrent ulceration, and progressive periodontal destruction</p> Case presentation <p>We report a 16-year-old female with hypothyroidism who presented with persistent gingival lesions and tooth mobility since early childhood after a mumps infection. Clinical and radiographic evaluation revealed generalized alveolar bone destruction. Histopathology confirmed LG with fibrinoid deposits. Hematological analysis showed markedly reduced plasminogen levels, measured using an ELISA-based assay, confirming the systemic deficiency. The patient was referred for ophthalmologic and genetic evaluation, targeting PLG gene mutations (K19E hotspot). She received chlorhexidine therapy with improved ulceration and reduced bleeding. At three-month follow-up, the lesions remained stable, and no ocular involvement was observed.</p> Conclusions <p>This case illustrates diagnostic challenges, differential considerations with aggressive periodontitis, and emphasizes the need for early recognition, multidisciplinary management, and systemic treatment to prevent severe complications such as blindness, infertility, or progressive periodontal morbidity.</p>

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Ligneous gingivitis: diagnostic and management challenges in a rare case

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月24日

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  • Metin Berk Kasapoglu,
  • Ahmet Turker,
  • Betul Gedik,
  • Necat Vakur Olgac

摘要

Introduction

Ligneous gingivitis (LG) is a rare manifestation of plasminogen deficiency characterized by woody fibrin-rich pseudomembranes, recurrent ulceration, and progressive periodontal destruction

Case presentation

We report a 16-year-old female with hypothyroidism who presented with persistent gingival lesions and tooth mobility since early childhood after a mumps infection. Clinical and radiographic evaluation revealed generalized alveolar bone destruction. Histopathology confirmed LG with fibrinoid deposits. Hematological analysis showed markedly reduced plasminogen levels, measured using an ELISA-based assay, confirming the systemic deficiency. The patient was referred for ophthalmologic and genetic evaluation, targeting PLG gene mutations (K19E hotspot). She received chlorhexidine therapy with improved ulceration and reduced bleeding. At three-month follow-up, the lesions remained stable, and no ocular involvement was observed.

Conclusions

This case illustrates diagnostic challenges, differential considerations with aggressive periodontitis, and emphasizes the need for early recognition, multidisciplinary management, and systemic treatment to prevent severe complications such as blindness, infertility, or progressive periodontal morbidity.