Abstract
Objective: Cluster of differentiation (CD14) is an important protein involved in activating toll-like receptors by bacterial components. It exists as either a transmembrane or soluble protein, called mCD14 or sCD14, respectively. Several studies show that CD14 regulates the inflammatory response to periodontal pathogens, and its expression is altered in periodontitis, an inflammatory disease of tooth-supporting tissues. It is the intent of this review to investigate the levels of expression of mCD14 and sCD14 in peripheral blood monocytes, saliva, gingival crevicular fluid, and gingival tissue biopsies in periodontitis patients. Methods: PubMed, Scopus, Ovid/Medline, Embase, and the Cochrane Library were consulted for the online literature search. To ensure methodical quality, titles and abstracts were reviewed in accordance to the PRISMA guidelines. Data extraction and evaluation of the full texts were executed in agreement with the GRADE approach. Results: This systematic review shows that mCD14 levels are decreased in peripheral blood monocytes of periodontitis patients in comparison to healthy patients, while sCD14 levels in sera, gingival crevicular fluid (GCF), and biopsies of periodontitis patients have a tendency to be increased in comparison to healthy controls. The evaluation of CD14 in gingival biopsies and periodontal tissues elucidated the fact that interpretation of the data obtained with qPCR, ELISA, and flow cytometry is questionable.
Highlights
Periodontitis is a multifactorial, inflammatory disease that causes the destruction of the periodontal tissues and, as the ultimate endpoint, can even lead to the loss of the tooth [1]
This review explicitly explores the levels of expression of mCD14 and sCD14 in peripheral blood monocytes, saliva, gingival crevicular fluid, and gingival tissue biopsies to allow a more in-depth understanding of the mechanism of periodontitis and provide information for future outcome measures for periodontal disease
Possible downregulation of mCD14 expression could be due to shedding regulated by P. gingivalis gingipains and cleaving of mCD14 from peripheral monocytes, resulting in a slower responsiveness of macrophages and monocytes as well as reduced phagocytosis and pathogen elimination of P. gingivalis
Summary
Periodontitis is a multifactorial, inflammatory disease that causes the destruction of the periodontal tissues and, as the ultimate endpoint, can even lead to the loss of the tooth [1]. According to a recent study by Tonetti, et al [2], the global burden of periodontal diseases remains high, with the most severe form affecting 11.2% of the world’s population [3]. Porphyromonas gingivalis, a gram-negative bacterium, is currently considered a keystone pathogen [4] and shows a strong association with periodontitis [5]. Recent studies have underscored that the pathogenicity of P. gingivalis lies in its constituents: Lipopolysaccharide (LPS), gingipains, and fimbriae/pili [6]. The human innate immune system comprises a family of pattern recognition receptors, termed toll-like receptors (TLRSs), which recognize various bacterial components and initiate the inflammatory reaction in response [7]. The recognition of bacterial components by TLRs is facilitated by numerous co-receptors, with the cluster of differentiation (CD) 14 being one of them [8]
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