Journal
JOURNAL OF DENTAL RESEARCH
Volume 93, Issue 3, Pages 231-237Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/0022034513507956
Keywords
congenital syndromes; leukocyte adhesion molecules; inflammation; bone marrow; neutrophil infiltration; periodontitis
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Funding
- National Institutes of Health, National Institute of Dental and Craniofacial Research [DE015254, DE021580, DE017138, DE021685]
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This review summarizes the current state of knowledge on neutrophil basic biology and discusses how the breakdown of neutrophil homeostasis affects periodontal health. The homeostasis of neutrophils is tightly regulated through coordinated bone marrow production, release into the circulation, transmigration to and activation in peripheral tissues, and clearance of senescent neutrophils. Dysregulation of any of these homeostatic mechanisms at any age can cause severe periodontitis in humans and animal models. Accordingly, both impaired and excessive neutrophil activity (in terms of numbers or immune function) can precipitate periodontitis. Neutrophil defects of congenital origin (e.g., congenital neutropenia, leukocyte adhesion deficiency, and Chediak-Higashi syndrome) are associated with cutaneous and systemic infections and early-onset forms of periodontitis affecting both the primary and permanent dentitions of children. However, the strong association between congenital neutrophil disorders and early-onset periodontitis is not currently adequately explained mechanistically. This suggests the operation of as-yet-unknown molecular mechanisms, although the available body of evidence leaves no doubt that neutrophils are integral to periodontal tissue homeostasis and health.
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