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Activation of oral keratinocytes by mercuric chloride: relevance to dental amalgam‐induced oral lichenoid reactions
Author(s) -
Little M.C.,
Watson R.E.B.,
Pemberton M.N.,
Griffiths C.E.M.,
Thornhill M.H.
Publication year - 2001
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1046/j.1365-2133.2001.04193.x
Subject(s) - mercury (programming language) , oral mucosa , chemistry , keratinocyte , amalgam (chemistry) , enzyme , dentistry , oral health , medicine , dermatology , in vitro , pharmacology , immunology , microbiology and biotechnology , pathology , biochemistry , biology , electrode , computer science , programming language
Background Despite the benefits of mercury‐containing amalgam dental fillings there are growing concerns regarding the potential adverse health effects arising from exposure to mercury released from fillings. In some individuals this process may result in a local lichenoid reaction of the oral mucosa. Objectives The aim of this study was to investigate the possibility that mercury salts released from amalgam fillings might act directly on oral keratinocytes to induce changes that could promote the development of such lesions. Methods In vitro experiments were performed in which normal oral and cutaneous keratinocytes were cultured in the presence of mercuric chloride (HgCl 2 ). ICAM‐1 expression and the release of cytokines was determined by enzyme‐linked immunosorbent assay techniques. T‐cell binding to HgCl 2 ‐pretreated keratinocytes was assessed using a colorimetric method. Results Subcytotoxic concentrations of HgCl 2 induced a concentration‐related increase in ICAM‐1 expression and consequent T‐cell binding on oral, but not cutaneous, keratinocytes. HgCl 2 also stimulated the release of low levels of tumour necrosis factor‐α and interleukin‐8 (but not RANTES), and inhibited the release of interleukin‐1α by oral keratinocytes. Conclusions This study provides evidence that oral keratinocytes may play an integral part in initiating the pathogenesis of amalgam‐induced lichenoid reactions.