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Localized cellular inflammatory responses to subcutaneously implanted dental mercury
V Nadarajah1, M E Neiders, A Aguirre
1Department of Oral Diagnostic Sciences, School of Dental Medicine, State University of New York at Buffalo 14214, USA.
Journal of Toxicology and Environmental Health
|October 11, 1996
Summary
Mercury exposure from dental amalgam causes inflammation in oral tissues. This study shows mercury leads to persistent chronic inflammation and changes in immune cells in rats.
Area of Science:
- Oral toxicology
- Immunopathology
- Biomaterials science
Background:
- Mercury accumulation and toxicity in oral tissues are known risks associated with dental amalgam restorations.
- Understanding the immune response to mercury exposure is crucial for assessing health risks.
Purpose of the Study:
- To histopathologically and immunocytochemically assess inflammatory responses to subcutaneously administered mercury in a rat model.
- To quantitate alterations in mononuclear cell subsets and major histocompatibility complex (MHC) class II determinant expression.
Main Methods:
- Utilized a rat model system for subcutaneous mercury administration.
- Employed histopathology and immunocytochemistry with monoclonal antibodies.
- Analyzed mononuclear cell subsets (monocytes, macrophages, T and B lymphocytes) and MHC class II (la) expression at various time intervals (2 days to 8 weeks).
Main Results:
- Observed acute inflammatory cell infiltration at 2-3 days, progressing to chronic inflammation persisting beyond 8 weeks.
- Detected significant alterations in monocyte, resident macrophage, and MHC class II expressing mononuclear cell populations at 1-2 weeks.
- Noted a sustained increase in resident macrophage numbers even after 8 weeks.
Conclusions:
- In situ mercury accumulation induces persistent chronic inflammation in oral tissues.
- Mercury exposure alters the expression of MHC class II determinants.
- Significant shifts in mononuclear cell subpopulations occur following mercury exposure, indicating a lasting immune response.