Open AccessAcantholysis may precede elevation of circulating anti‐desmoglein 3 antibody levels in pemphigus vulgaris presenting with desquamative gingivitis
Author(s) -
Endo Hiroyasu,
Rees Terry D.,
Niwa Hideo,
Kuyama Kayo,
Oshima Maya,
Serizawa Tae,
Tanaka Shigeo,
Komiya Masamichi,
Ito Takanori
Publication year - 2019
Publication title -
clinical and experimental dental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.464
H-Index - 9
ISSN - 2057-4347
DOI - 10.1002/cre2.174
Subject(s) - pemphigus vulgaris , acantholysis , medicine , autoantibody , desmoglein 3 , antibody , desmoglein 1 , pemphigus , desmoglein , immunology , autoimmune disease , pathology , dermatology
Pemphigus vulgaris (PV) is an autoimmune, blistering disease that affects the mucosa and skin. The current theory favors the concept that anti‐desmoglein (Dsg) 3 autoimmunity is the only pathogenic event needed to induce acantholysis. However, a few cases of active PV in the oral cavity had no detectable anti‐Dsg 3 antibody. The aim of this study was to evaluate the differences in clinical and laboratory findings, whether or not the anti‐Dsg 3 antibodies were present. This study was based on a retrospective review of 10 PV cases. The evaluation of the circulating autoantibody titers to Dsg 3 was conducted by using enzyme‐linked immunosorbent assay (ELISA). An index value of 20 or more was used as the cutoff for a positive reaction. Only five of the 10 PV cases had a positive Dsg 3 ELISA. There were no differences in clinical, cytological, histopathological, and direct immunofluorescence findings, whether or not the anti‐Dsg 3 antibodies were present. Of the five patients with a negative reaction at the time of diagnosis, the Dsg 3 ELISA became positive in the follow‐up period in three cases. In the remaining two cases, the Dsg 3 ELISA was consistently negative for 18 months. Dsg 3 ELISA was negative early in some PV cases. Therefore, PV acantholysis may precede the elevation of circulating anti‐Dsg 3 antibody levels. The diagnosis of PV should be considered based on comprehensive clinical, histopathological, and immunofluorescent criteria.