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Th17 Inflammation Model of Oropharyngeal Candidiasis in Immunodeficient Mice
Published on: February 18, 2015
Th17-cells in atopic dermatitis stimulate orthodontic root resorption.
K Yamada1, M Yamaguchi, M Asano
1Department of Orthodontics, Nihon University School of Dentistry at Matsudo, Chiba, Japan.
Oral Diseases
|January 3, 2013
Summary
Atopic dermatitis (AD) exacerbates orthodontic root resorption by increasing Th17 cell activity and related protein expression. This suggests AD patients are more susceptible to root damage during orthodontic tooth movement.
Area of Science:
- Immunology
- Orthodontics
- Dermatology
Background:
- Atopic dermatitis (AD) is an inflammatory skin condition.
- Orthodontic tooth movement can lead to root resorption.
- The link between AD and orthodontic root resorption is not fully understood.
Purpose of the Study:
- To investigate the role of atopic dermatitis in orthodontic root resorption.
- To analyze the expression of key proteins involved in root resorption in the context of AD.
Main Methods:
- Utilized a mouse model of atopic dermatitis and subjected them to excessive orthodontic force (OF).
- Measured protein expression of tartrate-resistant acid phosphatase (TRAP), IL-17, IL-6, and RANKL in the periodontal ligament (PDL).
- Investigated co-cultures of CD4+ cells from AD patients/healthy individuals and human PDL cells under compression force.
Main Results:
- Significantly increased immunoreactivity for TRAP, IL-17, IL-6, and RANKL was observed in the AD group.
- IL-17/CD4 co-localization confirmed the presence of Th17 cells.
- Elevated secretion and mRNA levels of IL-17, IL-6, and RANKL were found in AD patients compared to healthy individuals.
Conclusions:
- Th17 cells are implicated in the worsening of root resorption in AD.
- These findings may explain the increased susceptibility of AD patients to root resorption during excessive orthodontic force application.
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