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Isolation, Processing and Analysis of Murine Gingival Cells
Published on: July 2, 2013
Periodontitis and cytokine expression in CD14 deficient patients
K M McNamara1, S E Hall, R S Wilder
1Center for Oral and Systemic Diseases, University of North Carolina at Chapel Hill, School of Dentistry, Chapel Hill, NC 27516-7455, USA.
Journal of the International Academy of Periodontology
|April 2, 2003
Summary
Patients with paroxysmal nocturnal haemoglobinuria (PNH) have reduced inflammatory mediator release from monocytes. This study found no difference in periodontal disease but showed lower monocyte responses in PNH patients.
Area of Science:
- Immunology
- Periodontology
- Hematology
Background:
- Paroxysmal nocturnal haemoglobinuria (PNH) is characterized by a deficiency in monocytic CD14.
- Understanding inflammatory responses in PNH is crucial for managing associated conditions.
Purpose of the Study:
- To investigate the relationship between periodontal disease, local inflammatory mediators, and monocyte function in PNH patients.
- To compare inflammatory mediator levels in gingival crevicular fluid (GCF) and lipopolysaccharide (LPS)-stimulated monocytes between PNH patients and controls.
Main Methods:
- Cross-sectional, non-randomized study design.
- Assessment of periodontal status, GCF levels of PGE2 and IL-1beta.
- Measurement of inflammatory mediators released from LPS-stimulated peripheral blood monocytes in vitro.
Main Results:
- No significant differences in periodontal disease severity or GCF mediator levels were observed between PNH patients and controls.
- PNH monocytes secreted significantly lower levels of PGE2 and IL-1beta in response to LPS compared to controls.
- A positive association between monocytic and GCF levels of PGE2 was found across all study groups.
Conclusions:
- Monocytes deficient in glycosylphosphatidylinositol (GPI) anchor, as seen in PNH, exhibit reduced in vitro inflammatory mediator expression.
- While local GCF inflammation may not differ, intrinsic monocyte dysfunction in PNH impacts inflammatory mediator secretion.
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