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Updated: Aug 5, 2026

Granulocyte-dependent Autoantibody-induced Skin Blistering
Published on: October 12, 2012
Periodontal Involvement in Autoimmune Blistering Diseases: A Narrative Review
Teresita Sarquis1, Constanza Jiménez1, Sven Niklander1
1Facultad de Odontología, Dermoral Laboratory, Universidad Andrés Bello, Santiago 8370136, Región Metropolitana Chile.
Background:
Autoimmune blistering diseases (AIBDs) are characterized by autoantibody-mediated epithelial damage affecting the skin and mucous membranes. Among them, pemphigus vulgaris (PV) and mucous membrane pemphigoid (MMP) frequently involve the gingiva, most commonly presenting as desquamative gingivitis (DG). This chronic and painful gingival involvement may compromise oral hygiene and favor secondary inflammatory changes. Consequently, growing interest has focused on the periodontal status of patients with AIBDs and on associated oral microbiological findings.
Materials And Methods:
A narrative review was conducted using PubMed and Scopus to identify primary studies evaluating periodontal status in patients with AIBDs. Periodontal conditions were mainly assessed using conventional clinical parameters, including probing depth and clinical attachment loss, along with additional periodontal and oral hygiene indices.
Results:
Ten studies met the inclusion criteria. Most of them reported significantly worse periodontal status in AIBD compared to controls or DG-unaffected sites. In MMP, disease activity, duration, and DG involvement were associated with poorer periodontal parameters. Notably, adjusting for oral hygiene, as performed in only one study, rendered differences in PD and CAL non-significant, suggesting a potential confounding effect. However, the available evidence remains insufficient to support an independent link with clinically defined periodontitis. Only one study applied the 2017 World Workshop periodontitis classification, with similar conclusions. Microbiological data, limited to three MMP studies with heterogeneous methodologies, frequently detect periodontal pathogens associated with inflammatory tissue damage.
Conclusions:
Patients with AIBD tend to present worse periodontal status, likely due to pain limited oral hygiene and dysbiotic biofilms. These pathogens may amplify inflammation and perpetuate tissue destruction. Nevertheless, microbial profiles appear dynamic and influenced by disease activity and treatment. Recognizing this association is essential for early diagnosis and interdisciplinary management.
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